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Lomovsky, Alexey, Yulia Baburina, Irina Odinokova, Margarita Kobyakova, Yana Evstratova, Linda Sotnikova, Roman Krestinin, and Olga Krestinina. "Melatonin Can Modulate the Effect of Navitoclax (ABT-737) in HL-60 Cells." Antioxidants 9, no. 11 (November 18, 2020): 1143. http://dx.doi.org/10.3390/antiox9111143.
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Melatonin (N-acetyl-5-methoxytryptamine MEL) is an indolamine that has antioxidant, anti-inflammatory and anti-tumor properties. Moreover, MEL is capable of exhibiting both anti-apoptotic and pro-apoptotic effects. In the normal cells, MEL possesses antioxidant property and has an anti-apoptotic effect, while in the cancer cells it has pro-apoptotic action. We investigated the combined effect of MEL and navitoclax (ABT-737), which promotes cell death, on the activation of proliferation in acute promyelocytic leukemia on a cell model HL-60. The combined effect of these compounds leads to a reduction of the index of mitotic activity. The alterations in the level of anti- and pro-apoptotic proteins such as BclxL, Bclw, Mcl-1, and BAX, membrane potential, Ca2+ retention capacity, and ROS production under the combined action of MEL and ABT-737 were performed. We obtained that MEL in combination with ABT-737 decreased Ca2+ capacity, dropped membrane potential, increased ROS production, suppressed the expression of anti-apoptotic proteins such as BclxL, Bclw, and Mcl-1, and enhanced the expression of pro-apoptotic BAX. Since, MEL modulates autophagy and endoplasmic reticulum (ER) stress in cancer cells, the combined effect of MEL and ABT-737 on the expression of ER stress and autophagy markers was checked. The combined effect of MEL and ABT-737 (0.2 μM) increased the expression of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), leading to a decrease in the level of binding immunoglobulin protein (BIP) followed by an increase in the level of C/EBP homologous protein (CHOP). In this condition, the expression of ERO1 decreased, which could lead to a decrease in the level of protein disulfide isomerase (PDI). The obtained data suggested that melatonin has potential usefulness in the treatment of cancer, where it is able to modulate ER stress, autophagy and apoptosis.
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Qi, Chen, James A. Wheeler, Ashlie Pruett, and Phillip H. Pekala. "Expression of the RNA binding proteins, Mel-N1, Mel-N2, and Mel-N3 in adipose cells." Biochemical and Biophysical Research Communications 294, no. 2 (June 2002): 329–33. http://dx.doi.org/10.1016/s0006-291x(02)00472-2.
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Tolksdorf, Beatrice, Sina Zarif, Jürgen Eberle, Ahmet Hazini, Babette Dieringer, Franziska Jönsson, Florian Kreppel, Jens Kurreck, and Henry Fechner. "Silencing of Mcl-1 overcomes resistance of melanoma cells against TRAIL-armed oncolytic adenovirus by enhancement of apoptosis." Journal of Molecular Medicine 99, no. 9 (May 24, 2021): 1279–91. http://dx.doi.org/10.1007/s00109-021-02081-3.
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Abstract Arming of oncolytic viruses with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown as a viable approach to increase the antitumor efficacy in melanoma. However, melanoma cells may be partially or completely resistant to TRAIL or develop TRAIL resistance, thus counteracting the antitumor efficiency of TRAIL-armed oncolytic viruses. Recently, we found that TRAIL resistance in melanoma cells can be overcome by inhibition of antiapoptotic Bcl-2 protein myeloid cell leukemia 1 (Mcl-1). Here, we investigated whether the cytotoxicity of AdV-TRAIL, an oncolytic adenovirus, which expresses TRAIL after induction by doxycycline (Dox), can be improved in melanoma cells by silencing of Mcl-1. Two melanoma cell lines, the TRAIL-resistant MeWo and the TRAIL-sensitive Mel-HO were investigated. Treatment of both cell lines with AdV-TRAIL resulted in a decrease of cell viability, which was caused by an increase of apoptosis and necrosis. The proapoptotic effects were dependent on induction of TRAIL by Dox and were more pronounced in Mel-HO than in MeWo cells. SiRNA-mediated silencing of Mcl-1 resulted in a further significant decrease of cell viability and a further increase of apoptosis and necrosis in AdV-TRAIL-infected MeWo and Mel-HO cells. However, while in absolute terms, the effects were more pronounced in Mel-HO cells, in relative terms, they were stronger in MeWo cells. These results show that silencing of Mcl-1 represents a suitable approach to increase the cytotoxicity of a TRAIL-armed oncolytic adenovirus in melanoma cells. Key messages • Cytotoxicity of TRAIL-expressing adenovirus can be enhanced by silencing of Mcl-1. • The effect occurs in TRAIL-sensitive and TRAIL-resistant melanoma cells. • Increase of apoptosis is the main mechanism induced by Mcl-1 silencing.
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Shih, I., T. Wang, T. Wu, R. J. Kurman, and J. D. Gearhart. "Expression of Mel-CAM in implantation site intermediate trophoblastic cell line, IST-1, limits its migration on uterine smooth muscle cells." Journal of Cell Science 111, no. 17 (September 1, 1998): 2655–64. http://dx.doi.org/10.1242/jcs.111.17.2655.
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An immortalized implantation site intermediate trophoblastic cell line, IST-1, was established from a human placenta of 7 weeks gestation. IST-1 cells phenotypically resembled the implantation site intermediate trophoblastic cells in situ and expressed Mel-CAM (MUC 18 or CD146). Mel-CAM is a cell adhesion molecule belonging to the immunoglobulin gene superfamily. It is involved in heterophilic cell-cell adhesion and plays a role in several biological processes including tumor progression. We have previously shown that Mel-CAM was highly expressed in the intermediate (extravillous) trophoblast in the human implantation site. In this study we determined the function of Mel-CAM in the interaction of trophoblast and uterine smooth muscle in the implantation site. IST-1 cells failed to adhere to immobilized recombinant Mel-CAM in solid phase whereas the uterine smooth muscle cells did. The presence of the putative Mel-CAM ligand in smooth muscle cells was further supported by the finding that Mel-CAM-transfected but not the mock-transfected U937 leukemia cells bind to the confluent monolayer of uterine smooth muscle cells. IST-1 cells attached efficiently to the monolayer of the uterine smooth muscle cells and acquired a spindle-shaped morphology simulating smooth muscle cells. The cell binding was only marginally affected by Mel-CAM blocking antibodies. However, Mel-CAM blocking antibodies and recombinant Mel-CAM promoted cell migration from IST-1 cell spheroids on the smooth muscle monolayer. Taken together, our results suggest that IST-1 cells express Mel-CAM but not the putative Mel-CAM ligand. In contrast, the uterine smooth muscle cells express the putative Mel-CAM ligand which binds to Mel-CAM on the surface of the IST-1 cells. The interaction between Mel-CAM and its putative ligand confers a stationary phenotype for trophoblastic cells. These observations are consistent with an important role for Mel-CAM in limiting trophoblastic migration within the myometrium in the implantation site.
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Ulmer, J. B., E. D. Dolci, and G. E. Palade. "Glycophorin expression in murine erythroleukaemia cells." Journal of Cell Science 92, no. 2 (February 1, 1989): 163–71. http://dx.doi.org/10.1242/jcs.92.2.163.
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We have identified mature and putative precursor forms of glycophorins expressed in a virus-transformed murine erythroleukaemia (MEL) cell line and compared them with their normal erythroblast counterparts. The following differences were found: (1) the two major MEL cell glycophorins (apparent Mr values 29–30 and 43(x10(3] have greater mobility on polyacrylamide gels than their normal gp-3 and gp-2 counterparts, due at least in part to differences in their oligosaccharide sidechains; (2) MEL cell gp-3 consists of two discrete proteins; and (3) there are more potential glycophorin precursors in MEL cells than in normal mouse erythroblasts. Four proteins, with apparent Mr values of 21, 23, 26 and 27(x10(3], have tentatively been identified as glycophorin precursors, based on the following findings: (1) they are immunologically related to the glycophorins; and (2) their synthesis was induced by dimethyl sulphoxide coincidentally with that of gp-3 and gp-2. They do not appear to be glycoproteins, as evidenced by their lack of incorporation of [3H]galactose, [3H]glucosamine or [3H]mannose. In contrast, gp-3 and gp-2 incorporated [3H]galactose and [3H]glucosamine but not [3H]mannose. Partial characterization of the glycan moieties of MEL cell glycophorins indicates that they consist mostly of tri- and tetrasaccharides, with no indication of any N-linked chains. Hence, the glycans of MEL cell glycophorins are mostly (if not all) O-linked. Furthermore, treatment with N-glycanase did not change their electrophoretic mobility on polyacrylamide gels. MEL cell glycophorins were also shown to be modified by phosphoryl and fatty acyl groups.
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Foresti, M., L. Gaudio, and G. Geraci. "Selective gene mutation in MEL cells." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 265, no. 2 (February 1992): 195–202. http://dx.doi.org/10.1016/0027-5107(92)90048-7.
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Jiang, Yi, Ming Shen, Yuanyuan Chen, Yinghui Wei, Jingli Tao, and Honglin Liu. "Melatonin Represses Mitophagy to Protect Mouse Granulosa Cells from Oxidative Damage." Biomolecules 11, no. 7 (June 30, 2021): 968. http://dx.doi.org/10.3390/biom11070968.
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Various environmental stimuli, including oxidative stress, could lead to granulosa cell (GC) death through mitophagy. Recently, it was reported that melatonin (MEL) has a significant effect on GC survival during oxidative damage. Here, we found that MEL inhibited oxidative stress-induced mitophagy to promote GC survival. The loss of cell viability upon H2O2 exposure was significantly restored after MEL treatment. Concomitantly, MEL inhibited the activation of mitophagy during oxidative stress. Notably, blocking mitophagy repressed GC death caused by oxidative stress. However, MEL cannot further restore viability of cells treated with mitophagy inhibitor. Moreover, PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine-protein kinase, was inhibited by MEL during oxidative stress. As a result, the E3 ligase Parkin failed to translocate to mitochondria, leading to impaired mitochondria clearance. Using RNAi to knock down PINK1 expression, we further verified the role of the MEL-PINK1-Parkin (MPP) pathway in maintaining GC survival by suppressing mitophagy. Our findings not only clarify the protective mechanisms of MEL against oxidative damage in GCs, but also extend the understanding about how circadian rhythms might influence follicles development in the ovary. These findings reveal a new mechanism of melatonin in defense against oxidative damage to GCs by repressing mitophagy, which may be a potential therapeutic target for anovulatory disorders.
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Afanasieva, D. A., M. A. Baryshnikova, T. N. Zabotina, A. A. Borunova, O. S. Burova, E. Yu Rybalkina, A. A. Nikolina, and Z. G. Kadagidze. "CHARACTERISTICS OF MULTIDRUG RESISTANCE IN HUMAN SKIN MELANOMA CELL LINES." Russian Journal of Biotherapy 14, no. 4 (December 30, 2015): 39–44. http://dx.doi.org/10.17650/1726-9784-2015-14-4-39-44.
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MDR is the main obstacle to chemotherapy efficiency. MDR can grow in cancer cells even if only the one cytostatic agent will act. The aim of the nowadays work is to characterize MDR in metastatic human skin melanoma cell lines prepared in “N.N. Blokhin Russian Cancer Research Center”. pgpl70 expression was detected by immunofluorescence methods. mRNA of MDR gene was identified by Reverse Transcriptase- PCR( RT-PCR) method. Rhodamine 123 (Rhl23) emission has been evaluated by flow cyto- fluorimetiy, cytotoxic activity was estimated by MTT-tests. The cells sensitivity to Aianoza cytostatic effects has showed that mel Kor cells were sensitive to Aranoza acting, but mel Ibr and mel Mtp X were not. Mel Ibr cells had expressed pgpl70 from 35 to 50 per cent, it was detected by immunofluorescence reaction. Mel Kor and mel Mtp-X cells were not expressed P-glycoprotein. mRNA of genes responsible for multi-drug resistance - MDR1, BCRP, MRP1 and LRP (MVP) - were detected by PCR. mRNA of BCRP and MRP1 genes has low expression, barely visible stripes after 33 cycles in all cell lines samples. LRP (MVP) genes expression of mRNA, unfortunately, never managed to see. YB1 gene mRNA expression is well, it is typically for cancer cells. mRNA of gene was found in mel MtpX and mel Ibr subclones cell lines. Mel Kor cells didn't contain mRNA of MDR1 gene. The study of the Rhl23 emission from cells showed that mel Kor control cells had accumulated Rhl23 and didn't throw it out. Mel Ibr cell line accumulated Rhl23 and threw out the half part of it. Mel MtpX cell tine had accumulated the less part of Rhl23 and almost all were thrown out. Thus, the study shows that mel Kor cell tine that are sensitive to Aranoza doesn't express pgpl70, not contain mRNA of multi-chug resistance genes and does not throw Rhl23. Mel Ibr cells resistant to the Aranoza cytotoxic action express pgpl70 ,contain mRNA of MDR1 gene and throw out Rhl23. However, mel MtpX cell line resistant to Aranoza does not express pgpl70, but contains mRNA of MDR1 gene and actively throws out Rhl23.
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Kajiume, Teruyuki, Takashi Sato, and Masao Kobayashi. "The Expression of Polycomb Group Genes Products, Bmi1 and Mel-18, Regulate the Function of Murine Primitive Hematopoietic Cells." Blood 110, no. 11 (November 16, 2007): 1261. http://dx.doi.org/10.1182/blood.v110.11.1261.1261.
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Abstract The Polycomb group (PcG) genes (bmi1 and mel-18) known as negative control factors of the Hox gene is thought to regulate the differentiation and self-renewal of hematopoietic stem cells (HSCs). The loss of mel-18 results in the promotion of HSC self-renewal, and the increase of mel-18 expression inversely leads to the differentiation of HSCs. On the other hand, the loss of bmi1 does not lead to self-renewal activity of HSCs. In this study we examined the effect of expression of bmi1 and mel-18 on the role of function in murine HSCs. Lineage-negative, Sca1-positive, and cKit-positive primitive hematopoietic cells were purified and the expression of PcG protein was evaluated from the intra-nuclear distribution of PcG proteins. The Bmi1-positive hematopoietic cells barely contained Mel-18, and the Mel-18-positive cells barely contained Bmi1. the frequency of positive cells for both Bmi1 and Mel-18 was less than 0.5% of purified primitive hematopoietic cells. The expression levels of the PcG genes, bmi1 and mel-18, in HSCs were knocked down by siRNA and then gene expression was assessed by quantitative real-time PCR. The introduction of siRNA against bmi1 or mell-18 resulted in approximate 50 to 60% decrease of each gene expression without affecting another gene expression. Primary colony-forming activity of knocked down cells in response to stem cell factor, thrombopoietin and the ligand for flt3 was not affected by the induction of siRNA. However, secondary colony-forming activity from primary colony-forming cells in bmi1-knockdown cells was significantly decreased when compared with that of control cells. Conversely, the mel-18-knockdown cells significantly increased, suggesting that mel-18-knockdown cells are capable of proliferating activity. Finally, bone marrow reconstitutive activity was examined by using Ly5.1 and Ly5.2 system. While the bmi1-knockdown marrow cells decreased the reconstitutive activity, the mel-18-knockdown marrow cells showed the increase of engraftment activity after 6 months of transplantation. From these results, we consider that mel-18 and bmi1 have reciprocal functions in HSCs. Mammalian PcG protein complexes can be classified into two distinct types, Polycomb repressive complexes 1 and 2 (PRC1 and PRC2). The Mel-18 protein is a constituent of mammalian PRC1 together with M33, Bmi1 or rae28, and Scmh1. The Mel-18 protein is composed of 342 amino acids and the N-terminal region of the 102 amino acid, which includes the RING finger motif, shares 93% homology with Bmi1 protein. In addition, its secondary structure shows high homology with the Mel-18 and Bmi1 proteins. We hypothesized that the opposite function is expressed in HSCs because Mel-18 and Bmi1 share the same structure and compete when in the complex form. These results suggest that mel-18 and bmi1 have inverse function in HSCs and that the balance of Bmi1 and Mel-18 may regulate the fate of self-renewal and differentiation in HSCs.
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Vartanian, A. A., O. S. Burova, Kh S. Vishnyakova, I. V. Samoylenko, V. A. Misyurin, E. E. Egorov, O. O. Ryabaya, and M. A. Baryshnikova. "Vemurafenib resistant melanoma cells acquire mesenchymal stem cell-like properties." Advances in molecular oncology 6, no. 4 (December 15, 2019): 47–57. http://dx.doi.org/10.17650/2313-805x-2019-6-4-47-57.
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Background. Activating mutations in the BRAF gene leads to a constitutive activation of the MAPK signaling. The highly selective BRAFV600E inhibitor, vemurafenib, improves the overall survival of BRAF-mutant melanoma patients. However, despite the excellent results of response rate, the average duration of the response was short and acquired resistance develops in most BRAF mutated melanoma patients within a few months. Objective: to derive melanoma cell lines from surgical species of patients with BRAF mutant melanomas resistant to vemurafenib and to elucidate the mechanisms involved in acquired drug resistance.Materials and methods. Mel Ki and Mel F1702 melanoma cells were obtained from metastases of disseminated melanoma patients with BRAFV600E mutation. 2D tumor cell culture, MTT test, immunicytochemistry, flow cytometry, real-time polimerase chain reaction and osteogenic and adipocytic differentiation were used in the study.Results. We have derived two melanoma cell lines Mel Ki and Mel F1702 from tumor samples of patients with BRAFV600E mutation resistant to vemurafenib. These cells were homogenous and had fibroblastic morphology. The IC50 values for Mel Ki and Mel F1702 were 4.7 and 6.3 μM, respectively. The expression of cancer-testis antigens was not detected in both types of cells suggesting the stemness of Mel Ki and Mel F1702 melanoma cells. The immunophenotypic profile of the vemurafenib resistsant melanoma cells showed the expression of typical mesenchymal stem cells markers such as CD90, CD105 and CD44. In addition, we found that the melanoma cell lines derived from tumor resistant to vemurafenib differentiated into osteoblastand adipocyte-like cells. Conclusion. In this study we are offering an experimental evidence of the phenotypic transition of the vemurafenib-resistant melanoma cells into mesenchymal stem-like cells.
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Mohamed, Yasser, Mohamed A. Basyony, Nabila I. El-Desouki, Walied S. Abdo, and Mohammed A. El-Magd. "The potential therapeutic effect for melatonin and mesenchymal stem cells on hepatocellular carcinoma." BioMedicine 9, no. 4 (November 14, 2019): 24. http://dx.doi.org/10.1051/bmdcn/2019090424.
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Background/aim: Herein, we investigated the potential therapeutic effect of Melatonin (Mel) and/or mesenchymal stem cells (MSCs) on rat model of HCC. Materials and Methods: Female mature rats were divided into 5 groups (n = 10/group): normal (Nor), HCC group intraperitoneally injected with 200 mg/kg DEN, and 3 treated groups; HCC + Mel (Mel) group given Mel intraperitoneally 20 mg/kg, twice a week, HCC + MSCs (MSCs) group intravenously injected by 1 × 106 cells, and HCC + MSCs (Mel +MSCs) group. Results: Rats in HCC group showed most deteriorated effect in form of increased mortality and relative liver weight, elevated serum levels of ALT, AST, ALP, AFP and GGT in addition to increased pre-neoplastic nodules in liver tissues. Liver tissues of HCC group also exhibited lower level of apoptosis as indicated by decreased DNA fragmentation and expression of p53 caspase 9 and caspase 3 genes and increased PCNA immunoreactivity. Moreover, in this group the expression of IL6 and TGFβ1 genes was significantly upregulated. All these deleterious effects induced by DEN were reversed after administration of Mel and/ or MSCs with best improvement for the combined group (MSCs + Mel). Conclusions: These findings reveal a better therapeutic effect for MSCs when given with Mel and we attribute this beneficial effect, at least in part, to triggering apoptosis and targeting inflammation in HCC. Therefore, combined treatment with Mel and MSCs is recommended to enhance the therapeutic potential against HCC.
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Zhu, Mingpeng, Xueting Yuan, and Gang Ni. "Magneto-Electroluminescence in ITO/MEH-PPV:PEO:LiCF3SO3/Al Polymer Light-Emitting Electrochemical Cells." Micromachines 10, no. 8 (August 17, 2019): 546. http://dx.doi.org/10.3390/mi10080546.
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Magnetic field effects (MFE) have been extensively studied in organic light emitting diodes because of their potential application in organic spintronics devices. However, only a few studies on MFE in organic light-emitting electrochemical cells (LEC) have been reported. In this paper, magnetic field effects on the electroluminescence of an LEC device with the structure of ITO/MEH-PPV:PEO:LiCF3SO3/Al were studied at various temperatures. The luminance–current–voltage curves of the device shows the typical bi-polar characteristics of LECs; positive magnetic electroluminescence (MEL) was observed with a value of about 2.5% (B = 42 mT, 250 K), showing a Lorentzian line shape. With a decrease in temperature, the MEL value and the threshold voltage increased accordingly, below the possible mechanism is discussed.
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Cohen, J., C. Somma-Delpero, A. Verine, J. L. Codaccioni, and J. Boyer. "Increased monoester lipase activity in red blood cells during hyperthyroidism." Journal of Endocrinology 108, no. 3 (March 1986): 357–59. http://dx.doi.org/10.1677/joe.0.1080357.
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ABSTRACT Human red blood cells (RBC) contain a monoester lipase (MEL) activity which is tightly associated with the cell membrane and has its active site externally oriented, as inferred from the ability of the intact cell to hydrolyse an exogenously added lipid substrate. Membrane-bound MEL activity was measured by a radiochemical assay in intact RBC from 29 untreated hyperthyroid patients. The mean (±s.d.) MEL level was higher (P < 0·01) in these patients (1220 ± 212 mu./1012 RBC) than in the control group (1010 ± 120 mu./1012 RBC). There was no difference between men and women. The increase in MEL values was associated with significantly (P < 0·001) decreased values of mean cellular volume and mean cellular haemoglobin content. A continued study of 13 patients, who became euthyroid with treatment, showed a normalization of the MEL values in RBC. The increased lipolytic potency of RBC represents a new characteristic of hyperthyroid patients. Further exploration of the possible diagnostic or prognostic implications of this enzymatic change seems warranted. J. Endocr. (1986) 108, 357–359
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Kleszczyński, Konrad, Bernadetta Bilska, Agatha Stegemann, Damian Flis, Wieslaw Ziolkowski, Elżbieta Pyza, Thomas Luger, Russel Reiter, Markus Böhm, and Andrzej Slominski. "Melatonin and Its Metabolites Ameliorate UVR-Induced Mitochondrial Oxidative Stress in Human MNT-1 Melanoma Cells." International Journal of Molecular Sciences 19, no. 12 (November 28, 2018): 3786. http://dx.doi.org/10.3390/ijms19123786.
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Melatonin (Mel) is the major biologically active molecule secreted by the pineal gland. Mel and its metabolites, 6-hydroxymelatonin (6(OH)Mel) and 5-methoxytryptamine (5-MT), possess a variety of functions, including the scavenging of free radicals and the induction of protective or reparative mechanisms in the cell. Their amphiphilic character allows them to cross cellular membranes and reach subcellular organelles, including the mitochondria. Herein, the action of Mel, 6(OH)Mel, and 5-MT in human MNT-1 melanoma cells against ultraviolet B (UVB) radiation was investigated. The dose of 50 mJ/cm2 caused a significant reduction of cell viability up to 48%, while investigated compounds counteracted this deleterious effect. UVB exposure increased catalase activity and led to a simultaneous Ca++ influx (16%), while tested compounds prevented these disturbances. Additional analysis focused on mitochondrial respiration performed in isolated mitochondria from the liver of BALB/cJ mice where Mel, 6(OH)Mel, and 5-MT significantly enhanced the oxidative phosphorylation at the dose of 10−6 M with lower effects seen at 10−9 or 10−4 M. In conclusion, Mel, 6(OH)Mel and 5-MT protect MNT-1 cells, which express melatonin receptors (MT1 and MT2) against UVB-induced oxidative stress and mitochondrial dysfunction, including the uncoupling of oxidative phosphorylation.
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Giallongo, Cesarina, Piera La Cava, Daniele Tibullo, Nunziatina Parrinello, Provvidenza Guagliardo, Vittorio Del Fabro, Fabio Stagno, et al. "Imatinib Increases Cytotoxicity of Melphalan and Their Combination Allows An Efficient Killing of CML Cells." Blood 114, no. 22 (November 20, 2009): 4254. http://dx.doi.org/10.1182/blood.v114.22.4254.4254.
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Abstract Abstract 4254 BCR/ABL-positive cells are relatively resistant to chemotherapy and, in order to evaluate the effect of Imatinib (IM) in reverting drug-resistance, we evaluated on K562 the toxicity of 1 h exposure to cytosine arabinoside (ARA-C) 20 μM, hydroxyurea (HU) 100 μM, and melphalan (MEL) 20 μM, after a pre-treatment of 24 h with 1 μM IM. The doses of the drugs were similar to that achieved in the plasma after standard chemoterapeutic treatment. Cell viability was evaluated by ATP-lite at 24, 48 and 72 hs from beginning of drug-free condition. The combinations of IM plus MEL induced the highest cytotoxicity (P<0,001 at 24, 48 and 72 hs vs MEL alone) indicating that pre-treatment with IM increased K562 exposition to the genotoxic damage of MEL. We next analyzed effects on cell cycle and DNA damage by alkaline comet assay induced by this drug combination and we observed that DNA damage peaked at 48 h with IM/MEL combination. In addition, flow cytometry analysis showed that IM/MEL combination reduced the cell accumulation in G2/M phase induced by MEL (P<0.001 vs MEL), thus reducing the ability to DNA repair and recovery. These data indicate that inhibition of BCR/ABL activity by IM increased cell cytotoxicity of MEL by reducing the effectiveness of the DNA-repair pathways and decreasing the time for DNA repair at the G2/M checkpoint.. To ascertain that these results were linked to BCR/ABL inhibition, TonB.210, a cell line where the BCR-ABL expression is inducible by doxycycline (DOX), were treated in the same conditions. Only TonB.210 cultured with DOX were insensitive to MEL while IM/MEL combination reverted these drug resistance (P<0,001). In the final step we studied the sequential association IM/MEL on the proliferative potential of myeloid progenitors of 6 CML patients at diagnosis. IM/MEL combination increased the reduction of the overall number of colonies in comparison to IM alone (P<0.05 vs IM). In addition, the analysis on CFU-GM and BFU-E colonies by qRT-PCR demonstrated that the IM/MEL combination led to the highest reduction in the number of BCR/ABL positive colonies (P<0.01 vs IM). Therefore, our data indicate that the pre-inhibition of BCR/ABL activity by IM increases the toxicity of MEL and allows an efficient killing of human leukemic cells, thus suggesting new therapeutic combinations for CML patients Disclosures: No relevant conflicts of interest to declare.
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Yaacoub, Carole, Mariam Rifi, Dany El-Obeid, Hiba Mawlawi, Jean-Marc Sabatier, Bruno Coutard, and Ziad Fajloun. "The Cytotoxic Effect of Apis mellifera Venom with a Synergistic Potential of Its Two Main Components—Melittin and PLA2—On Colon Cancer HCT116 Cell Lines." Molecules 26, no. 8 (April 14, 2021): 2264. http://dx.doi.org/10.3390/molecules26082264.
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Colon carcinogenesis is ranked second globally among human diseases after cardiovascular failures. Bee venom (BV) has been shown to possess in vitro anticancer effects against several types of cancer cells. The two main biopeptides of Apis mellifera BV, namely, melittin (MEL) and phospholipase A2 (PLA2), are suspected to be the biomolecules responsible for the anticancer activity. The present work aims to evaluate the cytotoxic effect of the A. mellifera venom on human colon carcinoma cells (HCT116), and to assess the synergistic effect of MEL and PLA2 on these cells. After analyzing, through high-pressure liquid chromatography, the proportions of MEL and PLA2 on BV, we have established a cell viability assay to evaluate the effect of BV, MEL, PLA2, and a mixture of MEL and PLA2 on the HCT116 cells. Results obtained showed a strong cytotoxicity effect induced by the A. mellifera venom and to a lower extent MEL or PLA2 alone. Remarkably, when MEL and PLA2 were added together, their cytotoxic effect was greatly improved, suggesting a synergistic activity on HCT116 cells. These findings confirm the cytotoxic effect of the A. mellifera venom and highlight the presence of synergistic potential activities between MEL and PLA2, possibly inducing membrane disruption of HCT116 cancer cells. Altogether, these results could serve as a basis for the development of new anticancer treatments.
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Brydon, Lena, Florian Roka, Laurence Petit, Pierre de Coppet, Michèle Tissot, Perry Barrett, Peter J. Morgan, Christian Nanoff, A. Donny Strosberg, and Ralf Jockers. "Dual Signaling of Human Mel1a Melatonin Receptors via Gi2, Gi3, and Gq/11 Proteins." Molecular Endocrinology 13, no. 12 (December 1, 1999): 2025–38. http://dx.doi.org/10.1210/mend.13.12.0390.
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Abstract Mel 1a melatonin receptors belong to the superfamily of guanine nucleotide-binding regulatory protein (G protein)-coupled receptors. So far, interest in Mel 1a receptor signaling has focused mainly on the modulation of the adenylyl cyclase pathway via pertussis toxin (PTX)-sensitive G proteins. To further investigate signaling of the human Mel 1a receptor, we have developed an antibody directed against the C terminus of this receptor. This antibody detected the Mel 1a receptor as a protein with an apparent molecular mass of approximately 60 kDa in immunoblots after separation by SDS-PAGE. It also specifically precipitated the 2-[125I]iodomelatonin (125I-Mel)-labeled receptor from Mel 1a-transfected HEK 293 cells. Coprecipitation experiments showed that Gi2, Gi3, and Gq/11 proteins couple to the Mel 1a receptor in an agonist-dependent and guanine nucleotide-sensitive manner. Coupling was selective since other G proteins present in HEK 293 cells, (Gi1, Go, Gs, Gz, and G12) were not detected in receptor complexes. Coupling of the Mel 1a receptor to Gi and Gq was confirmed by inhibition of high-affinity 125I-Mel binding to receptors with subtype-selective G protein α-subunit antibodies. Gi2 and/or Gi3 mediated adenylyl cyclase inhibition while Gq/11 induced a transient elevation in cytosolic calcium concentrations in HEK 293 cells stably expressing Mel 1a receptors. Melatonin-induced cytosolic calcium mobilization via PTX-insensitive G proteins was confirmed in primary cultures of ovine pars tuberalis cells endogenously expressing Mel 1a receptors. In conclusion, we report the development of the first antibody recognizing the cloned human Mel 1a melatonin receptor protein. We show that Mel 1a receptors functionally couple to both PTX-sensitive and PTX-insensitive G proteins. The previously unknown signaling of Mel 1a receptors through Gq/11 widens the spectrum of potential targets for melatonin.
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Ohgama, Jun, Masahito Katoh, Mari Hirano, Hisashi Arase, Noriko Arase-Fukushi, Machiko Mishima, Kazuya Iwabuchi, Kazumasa Ogasawara, and Kazunori Onoé. "Functional studies on MEL-14+ and MEL-14− T cells in peripheral lymphoid tissues." Immunobiology 190, no. 3 (April 1994): 225–42. http://dx.doi.org/10.1016/s0171-2985(11)80271-8.
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Adam, Michael, Bao-Ling Tsay Adam, and Lloyd Wolfinbarger. "Ultrastructural characterization of the effects of beta-alanyl-melphalan in mouse Ehrlich ascites tumor cells and mouse liver cells." Proceedings, annual meeting, Electron Microscopy Society of America 50, no. 1 (August 1992): 642–43. http://dx.doi.org/10.1017/s0424820100123611.
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Beta-alanyl-melphalan (BAM) was demonstrated to have significant cancerocidal activity using both in vitro cultures and in vivo chemotherapy assays. Ultrastructural observations in the present study confirmed the antitumor activity of melphalan (MEL) and BAM. Results showed that the MEL affected the cellular elements causing marked cell damage both in mouse Ehrlich ascites tumor cells (MEATC) and mouse liver cells (MLC). BAM appeared to affect the cellular elements, with marked cell damage, only in MEATC, but not in the MLC. There were nuclear and cytoplasmic alterations in MEL and BAM treated MEATC, i.e. peripheral thickening of chromatin in nuclei, severe mitochondrial alterations, ribosome accumulation and autolysis phenomena which lead to the destruction of the subcellular structures.
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Macleod, K., and M. Plumb. "Derepression of mouse beta-major-globin gene transcription during erythroid differentiation." Molecular and Cellular Biology 11, no. 9 (September 1991): 4324–32. http://dx.doi.org/10.1128/mcb.11.9.4324.
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Functional analysis of the mouse beta-major-globin gene promoter has revealed a negative regulatory element (-100 to -250 bp) which represses promoter activity in mouse erythroleukemia (MEL) cells. Promoter activity is induced 14-fold during terminal differentiation of MEL cells. Three major in vitro binding sites for NF1 (-250 bp), GATA-1 (-212 bp), and a sequence at -165 bp (BB1) have been defined in this region. Site-directed mutagenesis of any one of the three sites resulted in a five- to sixfold up-regulation of promoter activity in uninduced MEL cells, but only three- to fourfold stimulation was observed from the mutant promoters during MEL cell terminal differentiation. This finding suggests that all three sites are required for repressor activity in uninduced MEL cells and that derepression occurs during MEL cell differentiation. BB1 DNA-binding activity decreases during MEL cell differentiation, suggesting a central role for this factor in modulating the effects of the repressor element. The BB1-binding factor also competes with the CCAAT-binding protein for binding the CCAAT motif. The fact that a reduced but significant stimulation of promoter activity during differentiation is observed in the absence of the repressor element raises the possibility that the BB1 factor also down-regulates transcription in undifferentiated MEL cells by displacing binding of CCAAT-binding protein to the proximal CCAAT motif.
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Macleod, K., and M. Plumb. "Derepression of mouse beta-major-globin gene transcription during erythroid differentiation." Molecular and Cellular Biology 11, no. 9 (September 1991): 4324–32. http://dx.doi.org/10.1128/mcb.11.9.4324-4332.1991.
Full textAbstract:
Functional analysis of the mouse beta-major-globin gene promoter has revealed a negative regulatory element (-100 to -250 bp) which represses promoter activity in mouse erythroleukemia (MEL) cells. Promoter activity is induced 14-fold during terminal differentiation of MEL cells. Three major in vitro binding sites for NF1 (-250 bp), GATA-1 (-212 bp), and a sequence at -165 bp (BB1) have been defined in this region. Site-directed mutagenesis of any one of the three sites resulted in a five- to sixfold up-regulation of promoter activity in uninduced MEL cells, but only three- to fourfold stimulation was observed from the mutant promoters during MEL cell terminal differentiation. This finding suggests that all three sites are required for repressor activity in uninduced MEL cells and that derepression occurs during MEL cell differentiation. BB1 DNA-binding activity decreases during MEL cell differentiation, suggesting a central role for this factor in modulating the effects of the repressor element. The BB1-binding factor also competes with the CCAAT-binding protein for binding the CCAAT motif. The fact that a reduced but significant stimulation of promoter activity during differentiation is observed in the absence of the repressor element raises the possibility that the BB1 factor also down-regulates transcription in undifferentiated MEL cells by displacing binding of CCAAT-binding protein to the proximal CCAAT motif.
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Clément, S., J. G. Delcros, H. S. Basu, G. Quash, L. J. Marton, and B. G. Feuerstein. "The structure of polyamine analogues determines haemoglobin production and cytotoxicity in murine erythroleukaemia cells." Biochemical Journal 309, no. 3 (August 1, 1995): 787–91. http://dx.doi.org/10.1042/bj3090787.
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The naturally occurring polyamine spermine induces haemoglobin synthesis in murine erythroleukaemia (MEL) cells. We have studied the ability of various polyamine analogues to inhibit cell growth and induce haemoglobin production. Polyamine analogues with free terminal amino groups were good inducers of haemoglobin production in MEL cells. Haemoglobin levels correlated with the number of positive charges: pentamines (five positive charges) were stronger inducers than tetramines (four positive charges). Compounds ethylated at their terminal amines were poor inducers of haemoglobin production but good inhibitors of MEL cell growth. These results provide evidence that polyamine analogues support specific biological functions of polyamines in MEL cells and suggest relationships between polyamine structure and function.
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Blank, Volker, Damien Lehalle, Louay Mardini, Mansouria Merad Boudia, Anna Derjuga, and Amy Moore. "Antagonistic Roles of ERK1/2 and p38 MAP Kinases in Hemoglobin Synthesis." Blood 106, no. 11 (November 16, 2005): 3636. http://dx.doi.org/10.1182/blood.v106.11.3636.3636.
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Abstract Murine erythroleukemia (MEL) cells provide a valuable model to study the molecular events leading to erythroid differentiation. Maturing erythroid cells synthesize large quantities of hemoglobin, a process requiring the coordinated synthesis of heme and globin. Here, we investigated the role of the ERK and p38 mitogen-activated protein kinase (MAPK) signaling pathways in the differentiation of MEL cells. We determined the effect of the MEK1/2 inhibitor U0126 that blocks the ERK1/2 pathway, and the p38 inhibitor SB202190 on the differentiation potential of MEL cells induced by hexamethylene bisacetamide (HMBA). We found that treatment of HMBA induced MEL cells with the ERK1/2 pathway inhibitor U0126 results in higher hemoglobin levels. Using a fluorometric assay, we determined that intracellular heme levels also increased. Immunoblot studies showed an increase in globin protein levels. In contrast, treatment of MEL cells with the p38 inhibitor SB202190 has the opposite effect, leading to decreased amounts of heme and hemoglobin. In addition, inhibition of the p38 pathways results in lower transferrin receptor levels. Our results suggest that the ERK1/2 and p38 pathways play antagonistic roles in HMBA induced erythroid differentiation in MEL cells. This data also provides a novel link between MAPK signaling and the regulation of heme biosynthesis and iron uptake in erythroid cells.
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Cowie, A., and R. M. Myers. "DNA sequences involved in transcriptional regulation of the mouse beta-globin promoter in murine erythroleukemia cells." Molecular and Cellular Biology 8, no. 8 (August 1988): 3122–28. http://dx.doi.org/10.1128/mcb.8.8.3122.
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We have developed a transient assay in murine erythroleukemia (MEL) cells to analyze the cis-acting sequence requirements for transcriptional regulation of the mouse beta-major-globin promoter. From deletion analysis, a fragment of the promoter region, from -106 to +26 relative to the RNA cap site, was found to be sufficient for regulated transcription in MEL cells following induction of differentiation by dimethyl sulfoxide. Single-base mutational analysis of this 132-base-pair promoter fragment identified three sequence elements required for transcription in MEL cells. These are the ATATAA sequence at -31 to -26, the CCAATC sequence between -77 and -72, and the GCCACACCC sequence between -95 and -87. In addition, we found a requirement for sequences adjacent to the CCAAT and ATATAA consensus motifs. Point mutations within the promoter did not abolish transcriptional regulation following induction of differentiation by dimethyl sulfoxide. However, mutations that resulted in reduced transcription levels in uninduced MEL cells gave similarly decreased levels in induced MEL cells.
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Cowie, A., and R. M. Myers. "DNA sequences involved in transcriptional regulation of the mouse beta-globin promoter in murine erythroleukemia cells." Molecular and Cellular Biology 8, no. 8 (August 1988): 3122–28. http://dx.doi.org/10.1128/mcb.8.8.3122-3128.1988.
Full textAbstract:
We have developed a transient assay in murine erythroleukemia (MEL) cells to analyze the cis-acting sequence requirements for transcriptional regulation of the mouse beta-major-globin promoter. From deletion analysis, a fragment of the promoter region, from -106 to +26 relative to the RNA cap site, was found to be sufficient for regulated transcription in MEL cells following induction of differentiation by dimethyl sulfoxide. Single-base mutational analysis of this 132-base-pair promoter fragment identified three sequence elements required for transcription in MEL cells. These are the ATATAA sequence at -31 to -26, the CCAATC sequence between -77 and -72, and the GCCACACCC sequence between -95 and -87. In addition, we found a requirement for sequences adjacent to the CCAAT and ATATAA consensus motifs. Point mutations within the promoter did not abolish transcriptional regulation following induction of differentiation by dimethyl sulfoxide. However, mutations that resulted in reduced transcription levels in uninduced MEL cells gave similarly decreased levels in induced MEL cells.
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Fernández-Calleja, Vanessa, Pablo Hernández, Jorge B. Schvartzman, Mario García de Lacoba, and Dora B. Krimer. "Differential gene expression analysis by RNA-seq reveals the importance of actin cytoskeletal proteins in erythroleukemia cells." PeerJ 5 (June 27, 2017): e3432. http://dx.doi.org/10.7717/peerj.3432.
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Development of drug resistance limits the effectiveness of anticancer treatments. Understanding the molecular mechanisms triggering this event in tumor cells may lead to improved therapeutic strategies. Here we used RNA-seq to compare the transcriptomes of a murine erythroleukemia cell line (MEL) and a derived cell line with induced resistance to differentiation (MEL-R). RNA-seq analysis identified a total of 596 genes (Benjamini–Hochberg adjustedp-value < 0.05) that were differentially expressed by more than two-fold, of which 81.5% (486/596) of genes were up-regulated in MEL cells and 110 up-regulated in MEL-R cells. These observations revealed that for some genes the relative expression of mRNA amount in the MEL cell line has decreased as the cells acquired the resistant phenotype. Clustering analysis of a group of genes showing the highest differential expression allowed identification of a sub-group among genes up-regulated in MEL cells. These genes are related to the organization of the actin cytoskeleton network. Moreover, the majority of these genes are preferentially expressed in the hematopoietic lineage and at least three of them,Was(Wiskott Aldrich syndrome),Btk(Bruton’s tyrosine kinase) andRac2, when mutated in humans, give rise to severe hematopoietic deficiencies. Among the group of genes that were up-regulated in MEL-R cells, 16% of genes code for histone proteins, both canonical and variants. A potential implication of these results on the blockade of differentiation in resistant cells is discussed.
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Sharkey, James T., Casey Cable, and James Olcese. "Melatonin Sensitizes Human Myometrial Cells to Oxytocin in a Protein Kinase Cα/Extracellularly Regulated Kinase-Dependent Manner." Molecular Endocrinology 24, no. 5 (May 1, 2010): 1106. http://dx.doi.org/10.1210/mend.24.5.9996.
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abstract Context: Studies have shown that labor occurs primarily in the night/morning hours. Recently, we identified the human myometrium as a target for melatonin (MEL), the neuroendocrine output signal coding for circadian night. Objective: The purpose of this study was to determine the signaling pathway underlying the effects of MEL on contractility and the contractile machinery in immortalized human myometrial cells. Design: To ascertain the signaling pathway of MEL leading to its effects on myometrial contractility in vitro, we performed gel retraction assays with cells exposed to iodo-MEL (I-MEL) with or without oxytocin and the Rho kinase inhibitor Y27632. I-MEL effects on inositol trisphosphate (IP3)/diacylglycerol (DAG)/protein kinase C (PKC) signaling were also investigated. Additionally, we assayed for caldesmon phosphorylation and ERK1/2 activation. Results: I-MEL was found to activate PKCα via the phospholipase C/IP3/DAG signaling pathway, which was confirmed by PKC enzyme assay. I-MEL did not affect myosin light chain phosphatase activity, and its effects on contractility were insensitive to Rho kinase inhibition. I-MEL did increase phosphorylation of ERK1/2 and caldesmon, which was inhibited by the MAPK kinase inhibitor PD98059 or the PKC inhibitor C1. Conclusions: MEL sensitizes myometrial cells to subsequent procontractile signals in vitro through activation of the phospholipase C/IP3/DAG signaling pathway, resulting in specific activation of PKCα and ERK1/2, thereby phosphorylating caldesmon, which increases actin availability for myosin binding and cross-bridging. In vivo, this sensitization would provide a mechanism for the increased nocturnal uterine contractility and labor that has been observed in late-term human pregnancy.
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Lannigan, D. A., J. B. Bennington, E. J. Cragoe, and P. A. Knauf. "Phenamil, an amiloride analogue, inhibits differentiation of Friend murine erythroleukemic cells." American Journal of Physiology-Cell Physiology 254, no. 1 (January 1, 1988): C122—C129. http://dx.doi.org/10.1152/ajpcell.1988.254.1.c122.
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Amiloride has been reported to inhibit Friend murine erythroleukemic (MEL) cell commitment to differentiate by inhibiting the MEL cell plasma membrane Na+-Ca2+ antiporter (R. L. Smith, I. G. Macara, R. Levenson, D. Housman, and L. Cantley. J. Biol. Chem. 257: 773-780, 1982). We therefore screened a series of amiloride analogues to determine whether a more potent and specific inhibitor of MEL cell differentiation could be found. In our experiments, as in those of Lubin (J. Cell. Physiol. 124: 539-544, 1985), amiloride itself did not inhibit MEL cell differentiation. However, we did find that the amiloride analogue phenamil reversibly inhibits dimethyl sulfoxide (DMSO)-induced MEL cell commitment to differentiate with a K1/2 of 2.5-5.0 microM (in plasma clot assay). At an extracellular concentration of 15 microM, phenamil inhibits commitment to differentiate by approximately 90% in the plasma clot assay while having a minimal effect on growth. Phenamil is not metabolized but is rapidly taken up by MEL cells. Phenamil was most effective as an inhibitor when present during the first 12 h of DMSO treatment, indicating that phenamil affects the early commitment process rather than later steps involved in hemoglobin synthesis. Phenamil does not, however, inhibit the early differentiation-induced decrease in [Na+]i and the concomitant drop in the Na+-K+ pump rate. A specific binding site for phenamil is suggested because some analogues in which the phenamil structure is slightly modified are unable to inhibit differentiation.
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Moravčík, Roman, Monika Okuliarová, Elena Kováčová, and Michal Zeman. "Diquat-induced cytotoxicity on Vero and HeLa cell lines: effect of melatonin and dihydromelatonin." Interdisciplinary Toxicology 7, no. 4 (December 1, 2014): 184–88. http://dx.doi.org/10.2478/intox-2014-0026.
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ABSTRACT Diquat dibromide is a moderately toxic contact herbicide belonging to the bipyridyl group of redox-active compounds that induce a strong oxidative damage. Melatonin (MEL) can protect against oxidative damage under in vivo conditions, probably through its antioxidative capacity and ability to induce expression of anti-oxidative enzymes. The objective of this study was to investigate effects of diquat on viability of Vero and HeLa cells and possible protective effects of MEL and its analogue 2,3-dihydromelatonin (DMEL). Cell viability was evaluated with the MTT test. First, we analyzed dose-dependent effects of diquat on cell viability using the concentration range of 0.1-100 μM. Second, we used the diquat dose which reduced cell viability by 50% and treated cells with either MEL or DMEL (both in the concentration range of 1-100 μM) in the presence or absence of diquat. In addition, effects of both diquat and MEL on oxidative stress in HeLa cells were measured by flow cytometry using 2’,7’-dichlorofluorescin diacetate. We confirmed the expected negative effects of diquat on viability of Vero and HeLa cells. Melatonin and DMEL were able to prevent diquat reduced viability of Vero cells in rather low concentrations (1 μM) and DMEL exerted substantially stronger protective effects than MEL. However in HeLa cells, we did not find the same effects and MEL even reduced their viability. Moreover, treatment of HeLa cells with high concentrations of MEL (100 μM) exaggerated the pro-oxidative effects of diquat. The results suggest that in addition to the expected anti-oxidative effects, MEL exerts a pro-oxidative action which is cell type and dose dependent
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Morozova, L. F., N. M. Suraeva, O. S. Burova, A. E. Barmashov, and M. A. Baryshnikova. "CHANGES IN THE MORPHOLOGICAL AND IMMUNOLOGICAL CHARACTERISTICS OF MEL CHER MELANOMA CELLS IN RESPONSE TO LOW CONCENTRATION OF EMBRYO CALF SERUM." Russian Journal of Biotherapy 15, no. 3 (September 30, 2016): 90–94. http://dx.doi.org/10.17650/1726-9784-2016-15-3-90-94.
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Background. Human melanoma cell line mel Cher have a different cell forms and is appraised for grade of differentiation as low-diffe-rentiation melanoma. Objective. The purpose of this study was development and characterization of subclone mel Cher 5C. Materials and methods. For received subclone mel Cher 5C was applied method of colony formation in conditions with low concentration of embryo calf serum (5 %). Then was carry out selection spindle-like cells, their long cultivation and estimate morphological and immunological characteristics. Results. Subclone mel Cher 5C cells differed for morphology from primary line mel Cher. This cells had spindle-like form and had capacity to form spherical type colony on the surface of monolayer during their growth. Subclone cells has more intensive growth compare with cells of primary line. Subclone cells had differences by immunological phenotype and didn’t expressed antigene HLA-DR. Conclusions. Subclone cells had a fusiform shape, in the growth process of the formed spheroid colonies monomorphic type, did not Express antigens of histocompatibility complex II.
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Yamada, Toshiyuki, Masaaki Abe, Toshinori Higashi, Hitomi Yamamoto, Fumiko Kihara-Negishi, Takuya Sakurai, Toshikazu Shirai, and Tsuneyuki Oikawa. "Lineage switch induced by overexpression of Ets family transcription factor PU.1 in murine erythroleukemia cells." Blood 97, no. 8 (April 15, 2001): 2300–2307. http://dx.doi.org/10.1182/blood.v97.8.2300.
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Abstract PU.1 is an Ets family transcription factor essential for myelomonocyte and B-cell development. We previously showed that overexpression of PU.1 in murine erythroleukemia (MEL) cells inhibits growth and erythroid differentiation and induces apoptosis of the cells. In an effort to identify target genes of PU.1 concerning these phenomena by using a messenger RNA differential display strategy, we found that some myeloid-specific and lymphoid-specific genes, such as the osteopontin gene, are transcriptionally up-regulated in MEL cells after overexpression of PU.1. We then found that expression of several myelomonocyte-specific genes, including the CAAT-enhancer-binding protein-α and granulocyte-macrophage colony-stimulating factor receptor genes, was induced in MEL cells after overexpression of PU.1. B-cell–specific genes were also examined, and expression of the CD19 gene was found to be induced. Expression of the myelomonocyte-specific proteins CD11b and F4/80 antigen but not the B-cell–specific proteins B220 and CD19 was also induced. After overexpression of PU.1, MEL cells became adherent and phagocytic and showed enhanced nitroblue tetrazolium reduction activity. Expression of myelomonocyte-specific and B-cell–specific genes was not induced when a mutant PU.1 with part of the activation domain deleted (a change found to inhibit erythroid differentiation of MEL cells) was expressed. These results indicate that PU.1 induces a lineage switch in MEL cells toward myelomonocytic cells and that its activation domain is essential for this effect. The results also suggest that the pathway of the lineage switch is distinct from that of inhibition of erythroid differentiation in MEL cells.
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Sherman, ML, TD Shafman, MS Colman, and DW Kufe. "Tiazofurin induction of mouse erythroleukemia cell hemoglobin production in the absence of commitment or changes in protooncogene expression." Blood 73, no. 2 (February 1, 1989): 431–34. http://dx.doi.org/10.1182/blood.v73.2.431.431.
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Abstract Tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193), is a synthetic nucleoside inhibitor of inosine monophosphate dehydrogenase and blocks guanine nucleotide biosynthesis. In the present study, we examined the effects of tiazofurin on mouse erythroleukemia (MEL) cell differentiation and protooncogene expression. Tiazofurin induced hemoglobin production in MEL cells in a concentration-dependent manner, as measured by an increase in benzidine staining. Northern blot analysis of MEL cells treated with 7 mumol/L tiazofurin demonstrated accumulation of both alpha- and beta-globin RNA transcripts. This induction of differentiation was blocked by the presence of exogenous guanosine (100 mumol/L). In contrast to the down- regulation of c-myc and c-myb RNA in MEL cells induced by dimethyl sulfoxide (DMSO) or hexamethylene bisacetamide (HMBA), there was no detectable change in levels of these transcripts after tiazofurin treatment. Furthermore, MEL cells induced by tiazofurin did not commit to terminal differentiation. These results suggest a role for guanine nucleotides, at least in part, in the regulation of MEL cell differentiation.
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Sherman, ML, TD Shafman, MS Colman, and DW Kufe. "Tiazofurin induction of mouse erythroleukemia cell hemoglobin production in the absence of commitment or changes in protooncogene expression." Blood 73, no. 2 (February 1, 1989): 431–34. http://dx.doi.org/10.1182/blood.v73.2.431.bloodjournal732431.
Full textAbstract:
Tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193), is a synthetic nucleoside inhibitor of inosine monophosphate dehydrogenase and blocks guanine nucleotide biosynthesis. In the present study, we examined the effects of tiazofurin on mouse erythroleukemia (MEL) cell differentiation and protooncogene expression. Tiazofurin induced hemoglobin production in MEL cells in a concentration-dependent manner, as measured by an increase in benzidine staining. Northern blot analysis of MEL cells treated with 7 mumol/L tiazofurin demonstrated accumulation of both alpha- and beta-globin RNA transcripts. This induction of differentiation was blocked by the presence of exogenous guanosine (100 mumol/L). In contrast to the down- regulation of c-myc and c-myb RNA in MEL cells induced by dimethyl sulfoxide (DMSO) or hexamethylene bisacetamide (HMBA), there was no detectable change in levels of these transcripts after tiazofurin treatment. Furthermore, MEL cells induced by tiazofurin did not commit to terminal differentiation. These results suggest a role for guanine nucleotides, at least in part, in the regulation of MEL cell differentiation.
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Coppola, J. A., J. M. Parker, G. D. Schuler, and M. D. Cole. "Continued withdrawal from the cell cycle and regulation of cellular genes in mouse erythroleukemia cells blocked in differentiation by the c-myc oncogene." Molecular and Cellular Biology 9, no. 4 (April 1989): 1714–20. http://dx.doi.org/10.1128/mcb.9.4.1714.
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Constitutive expression of the c-myc oncogene blocks dimethyl sulfoxide (DMSO)-induced differentiation of mouse erythroleukemia (MEL) cells. During the first 12 h of treatment with DMSO, MEL cells undergo a temporary decrease in the level of c-myc mRNA, followed by a temporary withdrawal from the cell cycle. We found the same shutoff of DNA synthesis during the first 12 to 30 h after DMSO induction in normal MEL cells (which differentiate) and in c-myc-transfected MEL cells (which do not differentiate). We also examined whether deregulated c-myc expression grossly interfered with the regulation of gene expression during MEL cell differentiation. We used run-on transcription assays to monitor the rate of transcription of four oncogenes (c-myc, c-myb, c-fos, and c-K-ras); all except c-K-ras showed a rapid but temporary decrease in transcription after induction in both c-myc-transfected and control cells. Finally, we found the same regulation of cytoplasmic mRNA expression in both types of cells for four oncogenes and three housekeeping genes associated with growth. We conclude that in the MEL cell system, the effects of deregulated c-myc expression do not occur through a disruption of cell cycle control early in induction, nor do they occur through gross deregulation of gene expression.
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Coppola, J. A., J. M. Parker, G. D. Schuler, and M. D. Cole. "Continued withdrawal from the cell cycle and regulation of cellular genes in mouse erythroleukemia cells blocked in differentiation by the c-myc oncogene." Molecular and Cellular Biology 9, no. 4 (April 1989): 1714–20. http://dx.doi.org/10.1128/mcb.9.4.1714-1720.1989.
Full textAbstract:
Constitutive expression of the c-myc oncogene blocks dimethyl sulfoxide (DMSO)-induced differentiation of mouse erythroleukemia (MEL) cells. During the first 12 h of treatment with DMSO, MEL cells undergo a temporary decrease in the level of c-myc mRNA, followed by a temporary withdrawal from the cell cycle. We found the same shutoff of DNA synthesis during the first 12 to 30 h after DMSO induction in normal MEL cells (which differentiate) and in c-myc-transfected MEL cells (which do not differentiate). We also examined whether deregulated c-myc expression grossly interfered with the regulation of gene expression during MEL cell differentiation. We used run-on transcription assays to monitor the rate of transcription of four oncogenes (c-myc, c-myb, c-fos, and c-K-ras); all except c-K-ras showed a rapid but temporary decrease in transcription after induction in both c-myc-transfected and control cells. Finally, we found the same regulation of cytoplasmic mRNA expression in both types of cells for four oncogenes and three housekeeping genes associated with growth. We conclude that in the MEL cell system, the effects of deregulated c-myc expression do not occur through a disruption of cell cycle control early in induction, nor do they occur through gross deregulation of gene expression.
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Sarre, T. F. "Presence of haemin-controlled eIF-2α kinases in both undifferentiated and differentiating mouse erythroleukaemia cells." Biochemical Journal 262, no. 2 (September 1, 1989): 569–74. http://dx.doi.org/10.1042/bj2620569.
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In rabbit reticulocytes, globin synthesis is regulated by a haemin-controlled translational inhibitor (HCI) which acts by phosphorylating the alpha-subunit of eukaryotic initiation factor 2 (eIF-2). With purified eIF-2 as substrate, haemin-controlled eIF-2 alpha kinases could be partially purified from cultured mouse erythroleukaemia cells (MEL cells), which can be induced in vivo to erythroid differentiation. The eIF-2 alpha kinases from both uninduced and induced MEL cells are clearly distinct from the double-stranded-RNA-activated eIF-2 alpha kinase described for many mammalian cell types. A rough quantitative estimation indicates that, on a per-cell basis, induced MEL cells contain the same amount of haemin-controlled eIF-2 alpha kinase activity as rabbit reticulocytes, whereas uninduced MEL cells contain about one-tenth as much. As to their chromatographic behavior on CM-Sephadex and DEAE-cellulose and their sensitivity towards physiological concentrations of haemin (5-10 microM), the eIF-2 alpha kinases from MEL cells are indistinguishable from HCI. They differ from HCI with respect to their response towards activating stimuli such as prolonged incubation at 37 degrees C or brief exposure to the thiol reagent N-ethylmaleimide.
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GENG, R., R. C. SUBEDI, S. LIANG, and T. D. NGUYEN. "DISCERNMENT OF POSSIBLE ORGANIC MAGNETIC FIELD EFFECT MECHANISMS USING POLYMER LIGHT-EMITTING ELECTROCHEMICAL CELLS." SPIN 04, no. 02 (June 2014): 1440010. http://dx.doi.org/10.1142/s2010324714400104.
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We report studies of magnetic field effect (MFE) in polymer light-emitting electrochemical cells (PLEC) using the "super-yellow" poly-(phenylene vynilene) (SY-PPV) polymer in vertical and planar device configurations. The purpose is to discern the existing MFE mechanisms in organic light emitting diodes (OLEDs) where the current and electroluminescence are strongly modulated by a small applied magnetic field. In particular, we investigate the mutual relationship between magneto-conductance (MC) and magneto-electroluminescence (MEL) by studying the role of polaron density dissociated from polaron pairs (PP) on these magnetic responses. In general, the dissociated polaron density is determined by the PP dissociation rate and the PP density. For the planar PLEC, which possesses a small dissociation rate, we observe small and negative MC at all applied voltages regardless of the emission intensity, while MEL becomes positive when electroluminescence quantum efficiency increases. The MC has a much narrower width than the MEL, indicating that the MC and MEL do not share a common origin. However, MC reverses and has the same width as MEL when the device is exposed to a threshold laser power. For the vertical PLEC, characterized by a large dissociation rate, MC and MEL are positive and have the same width. We discuss the results using the existing MFE mechanism in OLEDs. We show that the PP model can explain the positive MEL and MC, while the negative MC can be explained by the bipolaron model. Finally, we present a possibility to complete an all-organic PLEC magnetic sensor by using an inkjet printer.
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Ngai, J., V. C. Bond, B. J. Wold, and E. Lazarides. "Expression of transfected vimentin genes in differentiating murine erythroleukemia cells reveals divergent cis-acting regulation of avian and mammalian vimentin sequences." Molecular and Cellular Biology 7, no. 11 (November 1987): 3955–70. http://dx.doi.org/10.1128/mcb.7.11.3955.
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We studied the expression of transfected chicken and hamster vimentin genes in murine erythroleukemia (MEL) cells. MEL cells normally repress the levels of endogenous mouse vimentin mRNA during inducermediated differentiation, resulting in a subsequent loss of vimentin filaments. Expression of vimentin in differentiating MEL cells reflects the disappearance of vimentin filaments during mammalian erythropoiesis in vivo. In contrast, chicken erythroid cells express high levels of vimentin mRNA and vimentin filaments during terminal differentiation. We demonstrate here that chicken vimentin mRNA levels increase significantly in differentiating transfected MEL cells, whereas similarly transfected hamster vimentin genes are negatively regulated. In conjunction with in vitro nuclear run-on transcription experiments, these results suggest that the difference in vimentin expression in avian and mammalian erythropoiesis is due to a divergence of cis-linked vimentin sequences that are responsible for transcriptional and posttranscriptional regulation of vimentin gene expression. Transfected chicken vimentin genes produce functional vimentin protein and stable vimentin filaments during MEL cell differentiation, further demonstrating that the accumulation of vimentin filaments is determined by the abundance of newly synthesized vimentin.
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Ngai, J., V. C. Bond, B. J. Wold, and E. Lazarides. "Expression of transfected vimentin genes in differentiating murine erythroleukemia cells reveals divergent cis-acting regulation of avian and mammalian vimentin sequences." Molecular and Cellular Biology 7, no. 11 (November 1987): 3955–70. http://dx.doi.org/10.1128/mcb.7.11.3955-3970.1987.
Full textAbstract:
We studied the expression of transfected chicken and hamster vimentin genes in murine erythroleukemia (MEL) cells. MEL cells normally repress the levels of endogenous mouse vimentin mRNA during inducermediated differentiation, resulting in a subsequent loss of vimentin filaments. Expression of vimentin in differentiating MEL cells reflects the disappearance of vimentin filaments during mammalian erythropoiesis in vivo. In contrast, chicken erythroid cells express high levels of vimentin mRNA and vimentin filaments during terminal differentiation. We demonstrate here that chicken vimentin mRNA levels increase significantly in differentiating transfected MEL cells, whereas similarly transfected hamster vimentin genes are negatively regulated. In conjunction with in vitro nuclear run-on transcription experiments, these results suggest that the difference in vimentin expression in avian and mammalian erythropoiesis is due to a divergence of cis-linked vimentin sequences that are responsible for transcriptional and posttranscriptional regulation of vimentin gene expression. Transfected chicken vimentin genes produce functional vimentin protein and stable vimentin filaments during MEL cell differentiation, further demonstrating that the accumulation of vimentin filaments is determined by the abundance of newly synthesized vimentin.
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Delcros, J. G., B. Schwartz, S. Clément, H. S. Basu, L. J. Marton, and B. G. Feuerstein. "Spermine induces haemoglobin synthesis in murine erythroleukaemia cells." Biochemical Journal 309, no. 3 (August 1, 1995): 781–86. http://dx.doi.org/10.1042/bj3090781.
Full textAbstract:
The naturally occurring polyamine spermine induces haemoglobin synthesis in murine erythroleukaemia (MEL) cells. Haemoglobin production was accompanied by accumulation of cytoplasmic beta-globin mRNA and growth inhibition, but not by cell-cycle block or changes in cell volume. Hexamethylene-bisacetamide (HMBA), a well known differentiating agent, also induces haemoglobin production, but causes a G1 block and decreases cell volume. These findings indicate that HMBA and spermine affect MEL cells differently, even though both induce haemoglobin production.
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Hafid-Medheb, Khalid, Yvette Augery-Bourget, Marie-Nathalie Minatchy, Nicole Hanania, and Jacqueline Robert-Lézénès. "Bcl-XL is required for heme synthesis during the chemical induction of erythroid differentiation of murine erythroleukemia cells independently of its antiapoptotic function." Blood 101, no. 7 (April 1, 2003): 2575–83. http://dx.doi.org/10.1182/blood-2002-02-0478.
Full textAbstract:
Bcl-XL is essential for the survival and normal maturation of erythroid cells, especially at the late stage of erythroid differentiation. It remains unclear whether Bcl-XL serves only as a survival factor for erythroid cells or if it can induce a signal for differentiation. We have previously shown that dimethyl sulfoxide (DMSO) induction of erythroid differentiation in murine erythroleukemia (MEL) cells correlates with delay of apoptosis and specific induction of Bcl-XL. In this study, we investigate the contribution of Bcl-2 and Bcl-XL to survival and erythroid differentiation by generating stable MEL transfectants expressing these antiapoptotic regulators. Overexpression of Bcl-2 completely prevented apoptosis of MEL cells before and after DMSO induction, whereas overexpression of Bcl-XL only delayed it. Overexpression of Bcl-2 or Bcl-XL neither induced spontaneous erythroid differentiation nor accelerated DMSO-induced differentiation. Inhibition of Bcl-XL by antisense transcripts accelerated apoptosis in DMSO-treated MEL cells and blocked the synthesis of hemoglobin without altering the growth arrest associated with terminal erythroid differentiation. An antisense oligonucleotide to Bcl-XL did not induce apoptosis in MEL cells overexpressing Bcl-2 but greatly decreased their hemoglobin synthesis when treated with DMSO, suggesting that Bcl-XL is necessary for erythroid differentiation independently of its antiapoptotic function. Importantly, Bcl-XL antisense transcripts prevented heme synthesis but not globin mRNA induction in DMSO-treated MEL cells. Furthermore, inhibition of hemoglobin synthesis by Bcl-XLantisense was reversed by addition of exogenous hemin. Finally, Bcl-XL localized to mitochondria during MEL erythroid differentiation, suggesting that it may mediate a critical mitochondrial transport function related to heme biosynthesis.
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Stuve, L. L., and R. M. Myers. "A directly repeated sequence in the beta-globin promoter regulates transcription in murine erythroleukemia cells." Molecular and Cellular Biology 10, no. 3 (March 1990): 972–81. http://dx.doi.org/10.1128/mcb.10.3.972.
Full textAbstract:
We have identified a previously undetected cis-acting element in the mouse beta-major globin promoter region that is necessary for maximal transcription levels of the gene in the inducible preerythroid murine erythroleukemia (MEL) cell line. This element, termed the beta-globin direct-repeat element (beta DRE), consists of a directly repeated 10-base-pair sequence, 5'-AGGGCAG(G)AGC-3', that lies just upstream from the TATA box of the promoter. The beta DRE motif is highly conserved in all adult mammalian beta-globin promoter sequences known. Mutation of either single repeat alone caused less than a twofold decrease in transcript levels. However, simultaneous mutation of both repeated regions resulted in a ninefold decrease in accumulated transcripts when the gene was transiently transfected into MEL cells. Attachment of the beta DRE to a heterologous promoter had little effect on levels of accumulated transcripts initiated from the promoter in undifferentiated MEL cells but resulted in a threefold increase in transcript levels in induced (differentiated) MEL cells. Similarly, a comparison of the relative effects of mutations in the beta DRE in uninduced and induced MEL cells indicated that the element was more active in induced cells. The increase in beta DRE activity upon MEL cell differentiation and the more pronounced effects of mutations in both repeats of the beta DRE have implications for the mechanism of action of the element in regulating beta-globin transcription and for mutational studies of other repetitive or redundant transcription elements.
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Stuve, L. L., and R. M. Myers. "A directly repeated sequence in the beta-globin promoter regulates transcription in murine erythroleukemia cells." Molecular and Cellular Biology 10, no. 3 (March 1990): 972–81. http://dx.doi.org/10.1128/mcb.10.3.972-981.1990.
Full textAbstract:
We have identified a previously undetected cis-acting element in the mouse beta-major globin promoter region that is necessary for maximal transcription levels of the gene in the inducible preerythroid murine erythroleukemia (MEL) cell line. This element, termed the beta-globin direct-repeat element (beta DRE), consists of a directly repeated 10-base-pair sequence, 5'-AGGGCAG(G)AGC-3', that lies just upstream from the TATA box of the promoter. The beta DRE motif is highly conserved in all adult mammalian beta-globin promoter sequences known. Mutation of either single repeat alone caused less than a twofold decrease in transcript levels. However, simultaneous mutation of both repeated regions resulted in a ninefold decrease in accumulated transcripts when the gene was transiently transfected into MEL cells. Attachment of the beta DRE to a heterologous promoter had little effect on levels of accumulated transcripts initiated from the promoter in undifferentiated MEL cells but resulted in a threefold increase in transcript levels in induced (differentiated) MEL cells. Similarly, a comparison of the relative effects of mutations in the beta DRE in uninduced and induced MEL cells indicated that the element was more active in induced cells. The increase in beta DRE activity upon MEL cell differentiation and the more pronounced effects of mutations in both repeats of the beta DRE have implications for the mechanism of action of the element in regulating beta-globin transcription and for mutational studies of other repetitive or redundant transcription elements.
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Spielholz, C., ML Heaney, ME Morrison, AN Houghton, JC Vera, and DW Golde. "Granulocyte-macrophage colony-stimulating factor signals for increased glucose uptake in human melanoma cells." Blood 85, no. 4 (February 15, 1995): 973–80. http://dx.doi.org/10.1182/blood.v85.4.973.bloodjournal854973.
Full textAbstract:
While the primary targets for granulocyte-macrophage colony-stimulating factor (GM-CSF) are hematopoietic precursors and mature myeloid cells, GM-CSF receptors (GMR) are also found on normal tissues including placenta, endothelium, and oligodendrocytes as well as certain malignant cells. The function of GMR in these nonhematopoietic cells is unknown. We studied the function of GMR in human melanoma cell lines. Six of seven cell lines tested (clones 1–5 and 3.44 of SK-MEL-131, SK- MEL-188, SK-MEL-23, SK-MEL-22, and SK-MEL-22A) expressed mRNA encoding the membrane-bound and soluble isoforms of the alpha subunit of the GMR. Melanoma cell lines in early stages of differentiation expressed the largest quantities of alpha-subunit mRNA. Although five of these lines expressed trace levels of mRNA encoding the beta subunit of the GMR, Scatchard analysis of equilibrium binding data derived from three of the cell lines showed that they expressed only low-affinity GMR. Clones 3.44 and 1–5 of SK-MEL-131, and SK-MEL-188 cells expressed receptors with a dissociation constant (kd) for GM-CSF in the following ranges: 0.7 to 0.8, 1.2 to 1.8, and 0.4 to 0.8 nmol/L, respectively. GM- CSF stimulated glucose uptake in four of the melanoma cell lines expressing the alpha subunit, presumably through facilitative glucose transporters, as uptake was blocked by cytochalasin B but not cytochalasin E. Stimulation of glucose uptake was transient, with maximum stimulation occurring at approximately 30 minutes in the presence of 1 nmol/L GM-CSF. GM-CSF stimulated glucose uptake 1.4- to 2.0-fold but did not stimulate cell proliferation. These results suggest a metabolic role for the low-affinity GMR in melanoma cell lines and indicate that the alpha subunit of the GMR can signal for increased glucose uptake in nonhematopoietic tumor cells.
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Skarpidi, E., G. Vassilopoulos, G. Stamatoyannopoulos, and Q. Li. "Comparison of Expression of Human Globin Genes Transferred Into Mouse Erythroleukemia Cells and in Transgenic Mice." Blood 92, no. 9 (November 1, 1998): 3416–21. http://dx.doi.org/10.1182/blood.v92.9.3416.
Full textAbstract:
Abstract To examine whether transfer of γ globin genes into mouse erythroleukemia cells can be used for the analysis of regulatory elements of γ globin gene promoter, Aγ gene constructs carrying promoter truncations that have been previously analyzed in transgenic mice were used for production of stably transfected mouse erythroleukemia (MEL) cell clones and pools. We found that constructs, which contain a microlocus control region (μLCR) that efficiently protects globin gene expression from the effects of the position of integration in transgenic mice, display position-dependent globin gene expression in MEL cell clones. Aγ globin gene expression among MEL cell clones carrying the μLCR(−201)Aγ and μLCR(−382)Aγ gene constructs ranged 15.5-fold and 17.6-fold, respectively, and there was no correlation between theAγ mRNA levels and the copies of the transgene (r= .28, P = .18). There was significant variation in per copy Aγ globin gene expression among MEL cell pools composed of 10 clones, but not among pools composed of 50 clones, indicating that position effects are averaged in pools composed by large numbers of clones. The overall pattern of Aγ globin gene expression in MEL cell pools resembled that observed in transgenic mice indicating that MEL cell transfections can be used in the study ofcis elements controlling γ globin gene expression. MEL cell transfections, however, are not appropriate for investigation of cis elements, which either sensitize or protect the globin transgenes from position effects. © 1998 by The American Society of Hematology.
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Skarpidi, E., G. Vassilopoulos, G. Stamatoyannopoulos, and Q. Li. "Comparison of Expression of Human Globin Genes Transferred Into Mouse Erythroleukemia Cells and in Transgenic Mice." Blood 92, no. 9 (November 1, 1998): 3416–21. http://dx.doi.org/10.1182/blood.v92.9.3416.421k16_3416_3421.
Full textAbstract:
To examine whether transfer of γ globin genes into mouse erythroleukemia cells can be used for the analysis of regulatory elements of γ globin gene promoter, Aγ gene constructs carrying promoter truncations that have been previously analyzed in transgenic mice were used for production of stably transfected mouse erythroleukemia (MEL) cell clones and pools. We found that constructs, which contain a microlocus control region (μLCR) that efficiently protects globin gene expression from the effects of the position of integration in transgenic mice, display position-dependent globin gene expression in MEL cell clones. Aγ globin gene expression among MEL cell clones carrying the μLCR(−201)Aγ and μLCR(−382)Aγ gene constructs ranged 15.5-fold and 17.6-fold, respectively, and there was no correlation between theAγ mRNA levels and the copies of the transgene (r= .28, P = .18). There was significant variation in per copy Aγ globin gene expression among MEL cell pools composed of 10 clones, but not among pools composed of 50 clones, indicating that position effects are averaged in pools composed by large numbers of clones. The overall pattern of Aγ globin gene expression in MEL cell pools resembled that observed in transgenic mice indicating that MEL cell transfections can be used in the study ofcis elements controlling γ globin gene expression. MEL cell transfections, however, are not appropriate for investigation of cis elements, which either sensitize or protect the globin transgenes from position effects. © 1998 by The American Society of Hematology.
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Stoppa, Anne-Marie, N. Vey, C. Faucher, R. Bouabdallah, F. Viret, C. Chabannon, P. Ladaique, et al. "Stem Cell Transplantation in 281 Patients over 60 Years in Onco Hematologic Malignancies: A Single Center Experience." Blood 104, no. 11 (November 16, 2004): 5229. http://dx.doi.org/10.1182/blood.v104.11.5229.5229.
Full textAbstract:
Abstract From 06/1982 to 12/2003, 281 patients (163 male) received autologous (AuSCt) and/or allogeneic (AlloSCT) transplantations as part of first line treatment (61%) second line treatment(21%) or salvage therapy (17%). There were 140 multiple myelomas (including 3 amyloidosis), 62 lymphomas, 51 acute myeloid leukemias, 24 solid tumors and 4 chronic myeloid leukemias.Two hundred and sixty nine patients-median age: 64 y(60–77) - received Au SCT (28/261 received a second Au SCT in med of 2–7 months), 1patient (71 y) received a double syngeneic transplant,12 patients -median age: 62(60–68) received AlloSCT. Conditionning regimen (Cond reg) for the first Au SCT included Melphalan 140 mg/m² n=168; BEAM n=41; Melphalan 200mg/m² n=29; Mel Busulfan (8 to 16 mg/kg) or Mel TBI 8 grays n=18; Cytoxan 200mg/kg Melphalan1 40 n=9: TBI 8 Grays n=7; BCNU 600mg/m² n=3. Cond reg for the second Au SCT included Mel 200 n=20; Mel 140 n=4; BCU 600 n=4. Cond reg for the double syngeneic transplant were Mel 140 and Bu 8 Mel 140.Cond reg for the AlloSCT were Fludarabin/Busulfan/ATG (FBS) based reduced intensity regimen (RIC) in 11 cases. Ninety percent of the patients received peripheral blood stem cells-med 5,3.10*6CD34/kg (2–40)- 10% of the patients transplanted before 1994 received bone marrow cells. Tolerance was good with only 9/281 transplant related deaths: 5 sepsis/MOF in aplasia (D11–D21) 2 ARDS (D30–D80) 1 AGVH (D 60) 1 CGVH (3 years). Theses deaths occured in 4 ref MM( 2 renal instability,1 cardiac amyloidosis), 2 CR2 NHL, 1 OR1 MM, 1 stable MDS after FBS in 2 pts, BEAM in 2 pts, Mel 140 in 4 pts, Mel 200 (second transplant) in 1 pt. With a median follow up of 20 months from transplant,7/281 second cancers had occured: 1AML, 1ALL, 2 NSC pulmonary carcinoma, 1 colon cancer, 1uterin carcinoma, 1 melanoma; 2 of these 7 patients had died. One hundred and fifty eight patients had relapsed in a median of 11 months (1–92). Median survival for the 281 patients is 37 months without diference between pts older or younger than 65. Median survival for MM, NHL/HL, AML or ST are 40 months, 45 months, 18 months and 23 months respectively
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Shaw, Priyanka, Naresh Kumar, Dietmar Hammerschmid, Angela Privat-Maldonado, Sylvia Dewilde, and Annemie Bogaerts. "Synergistic Effects of Melittin and Plasma Treatment: A Promising Approach for Cancer Therapy." Cancers 11, no. 8 (August 3, 2019): 1109. http://dx.doi.org/10.3390/cancers11081109.
Full textAbstract:
Melittin (MEL), a small peptide component of bee venom, has been reported to exhibit anti-cancer effects in vitro and in vivo. However, its clinical applicability is disputed because of its non-specific cytotoxicity and haemolytic activity in high treatment doses. Plasma-treated phosphate buffered saline solution (PT-PBS), a solution rich in reactive oxygen and nitrogen species (RONS) can disrupt the cell membrane integrity and induce cancer cell death through oxidative stress-mediated pathways. Thus, PT-PBS could be used in combination with MEL to facilitate its access into cancer cells and to reduce the required therapeutic dose. The aim of our study is to determine the reduction of the effective dose of MEL required to eliminate cancer cells by its combination with PT-PBS. For this purpose, we have optimised the MEL threshold concentration and tested the combined treatment of MEL and PT-PBS on A375 melanoma and MCF7 breast cancer cells, using in vitro, in ovo and in silico approaches. We investigated the cytotoxic effect of MEL and PT-PBS alone and in combination to reveal their synergistic cytological effects. To support the in vitro and in ovo experiments, we showed by computer simulations that plasma-induced oxidation of the phospholipid bilayer leads to a decrease of the free energy barrier for translocation of MEL in comparison with the non-oxidized bilayer, which also suggests a synergistic effect of MEL with plasma induced oxidation. Overall, our findings suggest that MEL in combination with PT-PBS can be a promising combinational therapy to circumvent the non-specific toxicity of MEL, which may help for clinical applicability in the future.
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Reddy, P. M., and C. K. Shen. "Erythroid differentiation of mouse erythroleukemia cells results in reorganization of protein-DNA complexes in the mouse beta maj globin promoter but not its distal enhancer." Molecular and Cellular Biology 13, no. 2 (February 1993): 1093–103. http://dx.doi.org/10.1128/mcb.13.2.1093.
Full textAbstract:
Dimethyl sulfoxide (DMSO) induction of mouse erythroleukemia (MEL) cells represents a well-defined in vitro system of terminal erythroid differentiation. We have studied the molecular mechanisms of transcriptional activation of the mouse beta maj globin gene during MEL cell differentiation by analyzing nuclear factor-DNA interactions in vivo at the gene's upstream promoter and a distal enhancer, 5'HS-2. Genomic footprinting data indicate that three motifs, CAC, NF-E2/AP1, and GATA-1, of the 5'HS-2 enhancer are bound with nuclear factors in MEL cells both prior to and after DMSO induction. No obvious conformational change of these nuclear factor-DNA complexes could be detected upon terminal differentiation of MEL cells. On the other hand, DMSO induction of MEL cells leads to the formation of specific nuclear factor-DNA complexes at several transcriptional regulatory elements of the mouse beta maj globin upstream promoter. Our genomic footprinting data have interesting implications with respect to the molecular mechanisms of transcriptional regulation and chromatin change of the mouse beta maj globin gene during erythroid differentiation.
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Reddy, P. M., and C. K. Shen. "Erythroid differentiation of mouse erythroleukemia cells results in reorganization of protein-DNA complexes in the mouse beta maj globin promoter but not its distal enhancer." Molecular and Cellular Biology 13, no. 2 (February 1993): 1093–103. http://dx.doi.org/10.1128/mcb.13.2.1093-1103.1993.
Full textAbstract:
Dimethyl sulfoxide (DMSO) induction of mouse erythroleukemia (MEL) cells represents a well-defined in vitro system of terminal erythroid differentiation. We have studied the molecular mechanisms of transcriptional activation of the mouse beta maj globin gene during MEL cell differentiation by analyzing nuclear factor-DNA interactions in vivo at the gene's upstream promoter and a distal enhancer, 5'HS-2. Genomic footprinting data indicate that three motifs, CAC, NF-E2/AP1, and GATA-1, of the 5'HS-2 enhancer are bound with nuclear factors in MEL cells both prior to and after DMSO induction. No obvious conformational change of these nuclear factor-DNA complexes could be detected upon terminal differentiation of MEL cells. On the other hand, DMSO induction of MEL cells leads to the formation of specific nuclear factor-DNA complexes at several transcriptional regulatory elements of the mouse beta maj globin upstream promoter. Our genomic footprinting data have interesting implications with respect to the molecular mechanisms of transcriptional regulation and chromatin change of the mouse beta maj globin gene during erythroid differentiation.