Journal articles: 'Cancer, differentiation, NMR, colon cell lines'

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Park, Hyun, Nguyen Tuan, Joonseok Oh, Younglim Son, Mark Hamann, Robert Stone, Michelle Kelly, Sangtaek Oh, and MinKyun Na. "Sesterterpenoid and Steroid Metabolites from a Deep-Water Alaska Sponge Inhibit Wnt/β-Catenin Signaling in Colon Cancer Cells." Marine Drugs 16, no. 9 (August 27, 2018): 297. http://dx.doi.org/10.3390/md16090297.

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The Wnt/β-catenin signaling pathway is known to play critical roles in a wide range of cellular processes: cell proliferation, differentiation, migration and embryonic development. Importantly, dysregulation of this pathway is tightly associated with pathogenesis in most human cancers. Therefore, the Wnt/β-catenin pathway has emerged as a promising target in anticancer drug screening programs. In the present study, we have isolated three previously unreported metabolites from an undescribed sponge, a species of Monanchora (Order Poecilosclerida, Family Crambidae), closely related to the northeastern Pacific species Monanchora pulchra, collected from deep waters off the Aleutian Islands of Alaska. Through an assortment of NMR, MS, ECD, computational chemical shifts calculation, and DP4, chemical structures of these metabolites have been characterized as spirocyclic ring-containing sesterterpenoid (1) and cholestane-type steroidal analogues (2 and 3). These compounds exhibited the inhibition of β-catenin response transcription (CRT) through the promotion of β-catenin degradation, which was in part implicated in the antiproliferative activity against two CRT-positive colon cancer cell lines.

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Matusiak, Damien, Sarah Glover, Rajkumar Nathaniel, Kristina Matkowskyj, Jianxin Yang, and Richard V. Benya. "Neuromedin B and its receptor are mitogens in both normal and malignant epithelial cells lining the colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 4 (April 2005): G718—G728. http://dx.doi.org/10.1152/ajpgi.00156.2004.

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Bombesin-like peptides are uniformly thought to act as mitogens in cancer. Yet by studying human tissues, we have recently shown that bombesin and its mammalian homologue gastrin-releasing peptide act as morphogens, promoting tumor differentiation when aberrantly upregulated in colon cancer. In contrast, little is known about the bombesin-like peptide neuromedin B (NMB) and its receptor (NMB-R) in the human gastrointestinal tract. We therefore studied their presence and function in normal and malignant human colonic epithelia. Anti-NMB monoclonal antibodies were made against keyhole limpet hemocyanin (KLH)-conjugated human NMB, whereas anti-NMB-R antibodies were raised in rabbits against KLH-conjugated peptides corresponding to the third intracellular loop and COOH-terminal tail of the receptor protein. NMB antibody recognized two bands at ∼1.2 kDa and ∼1.5 kDa. NMB-R antibodies recognized a band at 80 kDa (predicted 43 kDa); whereas treatment with the deglycosylating agent peptide- N-glycosidase generated bands at 65, 47, and 43 kDa. By immunohistochemistry, both NMB and NMB-R were expressed in normal and cancerous colonic epithelial tissues. In cancer, the amount of NMB was similar to that expressed by proliferating epithelial cells located within the crypt. In contrast, NMB-R expression was increased in cancer, with higher levels detected in better differentiated tumor cells. To assess NMB function, proliferation was determined in the nonmalignant human colonic epithelial cell line NCM-460 and in the colon cancer cell lines Caco-2 and HT-29. Exogenously added NMB was 50–100% more efficacious than gastrin-releasing peptide in causing tumor cell proliferation, whereas only NMB increased NCM-460 cell proliferation. These findings indicate that NMB and its receptor are coexpressed by proliferating cells in which they act in an autocrine fashion with similar and modest potency in both normal and malignant colonic epithelial cells.

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Graziani, Vittoria, Nicoletta Potenza, Brigida D’Abrosca, Teresa Troiani, Stefania Napolitano, Antonio Fiorentino, and Monica Scognamiglio. "NMR Profiling of Ononis diffusa Identifies Cytotoxic Compounds against Cetuximab-Resistant Colon Cancer Cell Lines." Molecules 26, no. 11 (May 28, 2021): 3266. http://dx.doi.org/10.3390/molecules26113266.

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In the search of new natural products to be explored as possible anticancer drugs, two plant species, namely Ononis diffusa and Ononis variegata, were screened against colorectal cancer cell lines. The cytotoxic activity of the crude extracts was tested on a panel of colon cancer cell models including cetuximab-sensitive (Caco-2, GEO, SW48), intrinsic (HT-29 and HCT-116), and acquired (GEO-CR, SW48-CR) cetuximab-resistant cell lines. Ononis diffusa showed remarkable cytotoxic activity, especially on the cetuximab-resistant cell lines. The active extract composition was determined by NMR analysis. Given its complexity, a partial purification was then carried out. The fractions obtained were again tested for their biological activity and their metabolite content was determined by 1D and 2D NMR analysis. The study led to the identification of a fraction enriched in oxylipins that showed a 92% growth inhibition of the HT-29 cell line at a concentration of 50 µg/mL.

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Wang, Rui, In-Kiu Kwon, Muthusamy Thangaraju, Nagendra Singh, Kebin Liu, Philippe Jay, Franz Hofmann, Vadivel Ganapathy, and Darren D. Browning. "Type 2 cGMP-dependent protein kinase regulates proliferation and differentiation in the colonic mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 2 (July 15, 2012): G209—G219. http://dx.doi.org/10.1152/ajpgi.00500.2011.

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Signaling through cGMP has emerged as an important regulator of tissue homeostasis in the gastrointestinal tract, but the mechanism is not known. Type 2 cGMP-dependent protein kinase (PKG2) is a major cGMP effector in the gut epithelium, and the present studies have tested its importance in the regulation of proliferation and differentiation in the mouse colon and in colon cancer cell lines. Tissue homeostasis was examined in the proximal colon of Prkg2 −/− mice using histological markers of proliferation and differentiation. The effect of ectopic PKG2 on proliferation and differentiation was tested in vitro using inducible colon cancer cell lines. PCR and luciferase reporter assays were used to determine the importance of Sox9 downstream of PKG2. The colons of Prkg2 −/− mice exhibited crypt hyperplasia, increased epithelial apoptosis, and reduced numbers of differentiated goblet and enteroendocrine cells. Ectopic PKG2 was able to inhibit proliferation and induce Muc2 and CDX2 expression in colon cancer cells, but did not significantly affect cell death. PKG2 reduced Sox9 levels and signaling, suggesting possible involvement of this pathway downstream of cGMP in the colon. The work presented here demonstrates a novel antiproliferative and prodifferentiation role for PKG2 in the colon. These homeostatic functions of PKG2 were reproducible in colon cancer cells lines where downregulation of Sox9 is a possible mechanism. The similarities in phenotype between PKG2 and GCC knockout mice positions PKG2 as a likely mediator of the homeostatic effects of cGMP signaling in the colon.

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Kilanczyk, Ewa, Urszula Wasik, and Anna Filipek. "CacyBP/SIP phosphatase activity in neuroblastoma NB2a and colon cancer HCT116 cells." Biochemistry and Cell Biology 90, no. 4 (August 2012): 558–64. http://dx.doi.org/10.1139/o2012-011.

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Recently, we have reported that CacyBP/SIP could be a novel phosphatase for ERK1/2 kinase. In this work, we analyzed the CacyBP/SIP phosphatase activity toward ERK1/2 in 2 cell lines of different origin. We showed that overexpression of CacyBP/SIP in NB2a cells resulted in a lower level of phosphorylated ERK1/2 (P-ERK1/2) in the nuclear fraction while such overexpression in HCT116 cells had no effect on the level of P-ERK1/2. Moreover, we found that overexpression of CacyBP/SIP resulted in higher phosphatase activity in the nuclear fraction obtained from NB2a cells when compared with HCT116 cells. Using 2-D electrophoresis we showed that the pattern of spots representing CacyBP/SIP differed in these 2 cell lines and was probably due to a different phosphorylation state of this protein. We also established that after overexpression of CacyBP/SIP in NB2a cells, the amount of nuclear β-catenin was low, while it remained high in HCT116 cells. Since NB2a cells have differentiation potential and HCT116 cells do not, our data suggest that different activity of CacyBP/SIP in these 2 cell lines might affect the ERK1/2 pathway in the differentiation or proliferation processes.

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Bravard, A., J. Beaumatin, E. Dussaulx, T. Lesuffleur, A. Zweibaum, and C. Luccioni. "Modifications of the anti-oxidant metabolism during proliferation and differentiation of colon tumor cell lines." International Journal of Cancer 59, no. 6 (December 15, 1994): 843–47. http://dx.doi.org/10.1002/ijc.2910590622.

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Jordinson, M., I. El-Hariry, D. Calnan, J. Calam, and M. Pignatelli. "Vicia faba agglutinin, the lectin present in broad beans, stimulates differentiation of undifferentiated colon cancer cells." Gut 44, no. 5 (May 1, 1999): 709–14. http://dx.doi.org/10.1136/gut.44.5.709.

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BACKGROUNDDietary lectins can alter the proliferation of colonic cells. Differentiation is regulated by adhesion molecules which, being glycosylated, are targets for lectin binding.AIMSTo examine the effects of dietary lectins on differentiation, adhesion, and proliferation of colorectal cancer cells. METHODSDifferentiation was assessed in three dimensional gels, adhesion by aggregation assay, and proliferation by 3H thymidine incorporation. The role of the epithelial cell adhesion molecule (epCAM) was studied using a specific monoclonal antibody in blocking studies and Western blots. The human colon cancer cell lines LS174T, SW1222, and HT29 were studied.RESULTSThe cell line LS174T differentiated in the presence of Vicia fabaagglutinin (VFA) into gland like structures. This was inhibited by anti-epCAM monoclonal antibody. Expression of epCAM itself was unaffected. VFA as well as wheat germ agglutinin (WGA) and the edible mushroom lectin (Agaricus bisporus lectin, ABL) significantly aggregated LS174T cells but peanut agglutinin (PNA) and soybean agglutinin (SBA) did not. All lectins aggregated SW1222 and HT29 cells. Aggregation was blocked by the corresponding sugars. Aggregation of cells by VFA was also inhibited by anti-epCAM. VFA, ABL, and WGL inhibited proliferation of all the cell lines; PNA stimulated proliferation of HT29 and SW1222 cells. In competition studies all sugars blocked aggregation and proliferation of all cell lines, except that the addition of mannose alone inhibited proliferation.CONCLUSIONVFA stimulated an undifferentiated colon cancer cell line to differentiate into gland like structures. The adhesion molecule epCAM is involved in this. Dietary or therapeutic VFA may slow progression of colon cancer.

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Abu Almaaty, Ali H., Eslam E. M. Toson, El-Sherbiny H. El-Sayed, Mohamed A. M. Tantawy, Eman Fayad, Ola A. Abu Ali, and Islam Zaki. "5-Aryl-1-Arylideneamino-1H-Imidazole-2(3H)-Thiones: Synthesis and In Vitro Anticancer Evaluation." Molecules 26, no. 6 (March 18, 2021): 1706. http://dx.doi.org/10.3390/molecules26061706.

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A novel series of N-1 arylidene amino imidazole-2-thiones were synthesized, identified using IR, 1H-NMR, and 13C-NMR spectral data. Cytotoxic effect of the prepared compounds was carried out utilizing three cancer cell lines; MCF-7 breast cancer, HepG2 liver cancer, and HCT-116 colon cancer cell lines. Imidazole derivative 5 was the most potent of all against three cell lines. DNA flow cytometric analysis showed that, imidazoles 4d and 5 exhibit pre-G1 apoptosis and cell cycle arrest at G2/M phase. The results of the VEGFR-2 and B-Raf kinase inhibition assay revealed that compounds 4d and 5 displayed good inhibitory activity compared with reference drug erlotinib.

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Kato, Masashi, Tomomi Kusumi, Shigeki Tsuchida, Masanori Tanaka, Mutsuo Sasaki, and Hajime Kudo. "Induction of differentiation and peroxisome proliferator-activated receptor ? expression in colon cancer cell lines by troglitazone." Journal of Cancer Research and Clinical Oncology 130, no. 2 (February 1, 2004): 73–79. http://dx.doi.org/10.1007/s00432-003-0510-2.

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Wagner, Hans E., Carol Ann Toth, Glenn D. Steele, and Peter Thomas. "Metastatic potential of human colon cancer cell lines: relationship to cellular differentiation and carcinoembryonic antigen production." Clinical & Experimental Metastasis 10, no. 1 (January 1992): 25–31. http://dx.doi.org/10.1007/bf00163573.

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Möbus, VJ, R. Moll, CD Gerharz, DG Kieback, W. Weikel, G. Hoffmann, and R. Kreienberg. "Establishment of new ovarian and colon carcinoma cell lines: differentiation is only possible by cytokeratin analysis." British Journal of Cancer 69, no. 3 (March 1994): 422–28. http://dx.doi.org/10.1038/bjc.1994.78.

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Jones, Matthew F., Toshifumi Hara, Princy Francis, Xiao Ling Li, Sven Bilke, Yuelin Zhu, Marbin Pineda, Murugan Subramanian, Walter F. Bodmer, and Ashish Lal. "The CDX1–microRNA-215 axis regulates colorectal cancer stem cell differentiation." Proceedings of the National Academy of Sciences 112, no. 13 (March 16, 2015): E1550—E1558. http://dx.doi.org/10.1073/pnas.1503370112.

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The transcription factor caudal-type homeobox 1 (CDX1) is a key regulator of differentiation in the normal colon and in colorectal cancer (CRC). CDX1 activates the expression of enterocyte genes, but it is not clear how the concomitant silencing of stem cell genes is achieved. MicroRNAs (miRNAs) are important mediators of gene repression and have been implicated in tumor suppression and carcinogenesis, but the roles of miRNAs in differentiation, particularly in CRC, remain poorly understood. Here, we identified microRNA-215 (miR-215) as a direct transcriptional target of CDX1 by using high-throughput small RNA sequencing to profile miRNA expression in two pairs of CRC cell lines: CDX1-low HCT116 and HCT116 with stable CDX1 overexpression, and CDX1-high LS174T and LS174T with stable CDX1 knockdown. Validation of candidate miRNAs identified by RNA-seq in a larger cell-line panel revealed miR-215 to be most significantly correlated with CDX1 expression. Quantitative ChIP–PCR and promoter luciferase assays confirmed that CDX1 directly activates miR-215 transcription. miR-215 expression is depleted in FACS-enriched cancer stem cells compared with unsorted samples. Overexpression of miR-215 in poorly differentiated cell lines causes a decrease in clonogenicity, whereas miR-215 knockdown increases clonogenicity and impairs differentiation in CDX1-high cell lines. We identified the genome-wide targets of miR-215 and found that miR-215 mediates the repression of cell cycle and stemness genes downstream of CDX1. In particular, the miR-215 target gene BMI1 has been shown to promote stemness and self-renewal and to vary inversely with CDX1. Our work situates miR-215 as a link between CDX1 expression and BMI1 repression that governs differentiation in CRC.

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Said, Bastián, Iván Montenegro, Manuel Valenzuela, Yusser Olguín, Nelson Caro, Enrique Werner, Patricio Godoy, Joan Villena, and Alejandro Madrid. "Synthesis and Antiproliferative Activity of New Cyclodiprenyl Phenols against Select Cancer Cell Lines." Molecules 23, no. 9 (September 12, 2018): 2323. http://dx.doi.org/10.3390/molecules23092323.

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Six new cyclodiprenyl phenols were synthesized by direct coupling of perillyl alcohol and the appropriate phenol. Their structures were established by IR, HRMS and mainly NMR. Three human cancer cell lines—breast (MCF-7), prostate (PC-3) and colon (HT-29)—were used in antiproliferative assays, with daunorubicin and dunnione as positive controls. Results described in the article suggest that dihydroxylated compounds 2–4 and monohydroxylated compound 5 display selectivity against cancer cell lines, cytotoxicity, apoptosis induction, and mitochondrial membrane impairment capacity. Compound 2 was identified as the most effective of the series by displaying against all cancer cell lines a cytotoxicity close to dunnione antineoplastic agent, suggesting that the cyclodiprenyl phenols from perillyl alcohol deserve more extensive investigation of their potential medicinal applications.

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Chourasiya, Sumit S., Eppakayala Sreedhar, K. Suresh Babu, Nagula Shankaraiah, V. Lakshma Nayak, S. Ramakrishna, S. Sravani, and M. V. Basaveswara Rao. "Isolation, Synthesis and Biological Evaluation of Phenylpropanoids from the Rhizomes of Alpania galanga." Natural Product Communications 8, no. 12 (December 2013): 1934578X1300801. http://dx.doi.org/10.1177/1934578x1300801222.

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Bioactivity guided investigation of the DCM: MeOH (1:1) extract from the rhizomes of Alpinia galanga led to the isolation of phenylpropanoids (1–9) and their structures were established by 1H NMR, 13C NMR, IR and LC-MS/MS. These compounds have been evaluated for their in vitro anticancer activity against the human cancer cell lines A549 (lung cancer), Colo-205 (colon cancer), A431 (skin cancer), NCI H460 (lung cancer), PC-3 (prostate cancer), and HT-29 (colon cancer). Compounds 4 and 9 showed potent anticancer activity (ranging from 1.3–19.7 μg/mL) against all the tested cancer cell lines. In addition, an asymmetric synthesis of acetoxychavicol acetate (1) and trans-p-coumaryl alcohol (4) has been accomplished in six steps starting from readily available p-hydroxybenzaldehyde for the first time. Grignard reaction and Sharpless kinetic resolution reactions were utilized as the key steps to install the basic core.

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Hoai, Tran Thanh, Phan Thi Yen, Tran Thi Bich Dao, Luu Hai Long, Duong Xuan Anh, Luu Hai Minh, Bui Quoc Anh, and Nghiem Thi Thuong. "Evaluation of the Cytotoxic Effect of Rutin Prenanoemulsion in Lung and Colon Cancer Cell Lines." Journal of Nanomaterials 2020 (November 18, 2020): 1–11. http://dx.doi.org/10.1155/2020/8867669.

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In this work, prenanoemulsion of rutin was prepared using PEG and Tween as emulsifiers via homogenization and evaporation techniques. The particle size of rutin was investigated with high-resolution transmission electron microscopy (HR-TEM); particle size distribution and its chemical structure were analysed by nuclear magnetic resonance (NMR) and Fourier transformed infrared (FT-IR) spectroscopy. It was found that rutin in the prenanoemulsion has excellent solubility in water with the size approximately 15 nm. The chemical structure of nanorutin in prenanoemulsion was identical to that of the pure rutin. It suggested that there is no chemical modification of rutin in the prenanoemulsion. From high-performance liquid chromatography (HPLC), the amount of rutin in the prenanoemulsion was determined to be 9.27%. The cytotoxic effect of rutin in the preemulsion was investigated via in vitro tests to determine rutin’s efficacy in A549 lung cancer cell and colon cancer cell treatment. The results demonstrated that rutin in the prenanoemulsion could inhibit A549 lung cancer cells and colon cancer cells efficiently.

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Dommann, Noëlle, Daniel Sánchez-Taltavull, Linda Eggs, Fabienne Birrer, Tess Brodie, Lilian Salm, Felix Alexander Baier, et al. "The LIM Protein Ajuba Augments Tumor Metastasis in Colon Cancer." Cancers 12, no. 7 (July 15, 2020): 1913. http://dx.doi.org/10.3390/cancers12071913.

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Colorectal cancer, along with its high potential for recurrence and metastasis, is a major health burden. Uncovering proteins and pathways required for tumor cell growth is necessary for the development of novel targeted therapies. Ajuba is a member of the LIM domain family of proteins whose expression is positively associated with numerous cancers. Our data shows that Ajuba is highly expressed in human colon cancer tissue and cell lines. Publicly available data from The Cancer Genome Atlas shows a negative correlation between survival and Ajuba expression in patients with colon cancer. To investigate its function, we transduced SW480 human colon cancer cells, with lentiviral constructs to knockdown or overexpress Ajuba protein. The transcriptome of the modified cell lines was analyzed by RNA sequencing. Among the pathways enriched in the differentially expressed genes, were cell proliferation, migration and differentiation. We confirmed our sequencing data with biological assays; cells depleted of Ajuba were less proliferative, more sensitive to irradiation, migrated less and were less efficient in colony formation. In addition, loss of Ajuba expression decreased the tumor burden in a murine model of colorectal metastasis to the liver. Taken together, our data supports that Ajuba promotes colon cancer growth, migration and metastasis and therefore is a potential candidate for targeted therapy.

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Herreros, A. G., M. Fabre, E. Batlle, C. Balague, and F. X. Real. "The tumor promoter 12-O-tetradecanoylphorbol-13-acetate blocks differentiation of HT-29 human colon cancer cells." Journal of Cell Science 105, no. 4 (August 1, 1993): 1165–72. http://dx.doi.org/10.1242/jcs.105.4.1165.

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Recently developed HT-29-derived cell lines, which display variable differentiated phenotypes provide an invaluable opportunity to analyze the mechanism by which cell differentiation is regulated in the intestine. We have studied the effects of the tumor promoter 12-O-tetradecanoylphorbol-13- acetate (TPA) in the differentiation phenotype of mucus-secreting (HT-29 M6) and absorptive (HT-29 M3) cells. TPA prevented the accumulation of differentiation markers such as dipeptidylpeptidase IV, villin or mucins, down-regulated the expression of these molecules in post-confluent differentiated cell cultures and induced the loss of the functional integrity of the tight junction in the monolayer (i.e. decreased transepithelial resistance and inhibited dome formation). These effects were mediated by activation of protein kinase C (PK-C), as demonstrated using the specific inhibitor GF109203x. Analysis by immunoblotting of the PK-C isoforms present in HT-29 M6 cells revealed that the most abundant TPA-sensitive isoform was PK-C epsilon, although low levels of cPK-C were also detected. Further studies are necessary to elucidate the role of the different PK-C isoforms in the differentiation of HT-29 cells.

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Dehm, Scott M., and Keith Bonham. "SRCgene expression in human cancer: the role of transcriptional activation." Biochemistry and Cell Biology 82, no. 2 (April 1, 2004): 263–74. http://dx.doi.org/10.1139/o03-077.

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Human pp60c-Src(or c-Src) is a 60 kDa nonreceptor tyrosine kinase encoded by the SRC gene and is the cellular homologue to the potent transforming v-Src viral oncogene. c-Src functions at the hub of a vast array of signal transduction cascades that influence cellular proliferation, differentiation, motility, and survival. c-Src activation has been documented in upwards of 50% of tumors derived from the colon, liver, lung, breast, and pancreas. Therefore, a major focus has been to understand the mechanisms of c-Src activation in human cancer. Early studies concentrated on post-translational mechanisms that lead to increased c-Src kinase activity, which often correlated with overexpression of c-Src protein. More recently, the discovery of an activating SRC mutation in a small subset of advanced colon tumors has been reported. In addition, elevated SRC transcription has been identified as yet another mechanism contributing significantly to c-Src activation in a subset of human colon cancer cell lines. Interestingly, histone deacetylase (HDAC) inhibitors, agents with well-documented anti-cancer activity, repress SRC transcription in a wide variety of human cancer cell lines. Analysis of the mechanisms behind HDAC inhibitor mediated repression could be utilized in the future to specifically inhibit SRC gene expression in human cancer.Key words: c-Src, tyrosine kinase, gene expression, transcription, colon cancer.

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Taylor, C. W., Y. S. Kim, K. E. Childress-Fields, and L. C. Yeoman. "Sensitivity of nuclear c-myc levels and induction to differentiation-inducing agents in human colon tumor cell lines." Cancer Letters 62, no. 2 (February 1992): 95–105. http://dx.doi.org/10.1016/0304-3835(92)90179-y.

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Tran, Chau P., Mary Familari, Lorraine M. Parker, Robert H. Whitehead, and Andrew S. Giraud. "Short-chain fatty acids inhibit intestinal trefoil factor gene expression in colon cancer cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 1 (July 1, 1998): G85—G94. http://dx.doi.org/10.1152/ajpgi.1998.275.1.g85.

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Intestinal trefoil factor (ITF) gene expression was detected in five colon cancer cell lines. ITF was synthesized by mucous cells of LIM 1215 and LIM 1863 lines, from which it is secreted constitutively. The ITF mRNA transcript was estimated to be 0.6 kb. In LIM 1215 cells, the expression of ITF was potently and dose-dependently inhibited by short-chain fatty acids (butyrate > propionate > acetate) within 8 h of application. The inhibitory effect of butyrate was ablated by actinomycin D and preceded its effects on differentiation of LIM 1215 cells as indicated by induction of alkaline phosphatase activity and counting of periodic acid-Schiff-positive cells. The human ITF promoter contained an 11-residue consensus sequence with high homology to the butyrate response element of the cyclin D1 gene. Mobility shift assays show specific binding of this response element to nuclear protein extracts of LIM 1215 cells. We conclude that butyrate inhibits ITF expression in colon cancer cells and that this effect may be mediated transcriptionally and independently of its effects on differentiation.

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Bernard-Perrone, Françoise, Jacqueline Carrere, Wanda Renaud, Christine Moriscot, Karine Thoreux, Patrice Bernard, Alain Servin, Daniel Balas, and Françoise Senegas-Balas. "Pancreatic trypsinogen I expression during cell growth and differentiation of two human colon carcinoma cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 6 (June 1, 1998): G1077—G1086. http://dx.doi.org/10.1152/ajpgi.1998.274.6.g1077.

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Pancreatic trypsin has been found to induce tight junction or dome formation in some colon cancer cell lines (HT-29, Caco-2), and a tumor-associated trypsinogen, trypsinogen type II, has been isolated from another colon cancer cell line (COLO 205). We have tried to determine if trypsinogen is present and how its expression varies during cell culture in HT-29 Glc+/− and Caco-2 cells, which exhibit enterocytic differentiation, and in HT-29 Glc+ cells, which never differentiate. Trypsinogen mRNA presence and expression were demonstrated in these cells by mRNA hybridization, RT-PCR, cytoimmunofluorescence, Western immunoblot analysis, and gel filtration. Trypsinogen was found to be trypsinogen type I and was mainly in zymogen form in culture media. Differentiating cells exhibited variations in trypsinogen I expression, but cells that remained undifferentiated did not. In the differentiated cells, a high and transient peak in trypsinogen I expression was observed during the first steps of differentiation.

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Beck, Stayce E., Barbara H. Jung, Antonio Fiorino, Jessica Gomez, Eunice Del Rosario, Betty L. Cabrera, Sherry C. Huang, Jimmy Y. C. Chow, and John M. Carethers. "Bone morphogenetic protein signaling and growth suppression in colon cancer." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 1 (July 2006): G135—G145. http://dx.doi.org/10.1152/ajpgi.00482.2005.

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Bone morphogenetic proteins (BMPs) are members of the transforming growth factor-β superfamily, which utilize BMP receptors and intracellular SMADs to transduce their signals to regulate cell differentiation, proliferation, and apoptosis. Because mutations in BMP receptor type IA ( BMPRIA) and SMAD4 are found in the germline of patients with the colon cancer predisposition syndrome juvenile polyposis, and because the contribution of BMP in colon cancers is largely unknown, we examined colon cancer cells and tissues for evidence of BMP signaling and determined its growth effects. We determined the presence and functionality of BMPR1A by examining BMP-induced phosphorylation and nuclear translocation of SMAD1; transcriptional activity via a BMP-specific luciferase reporter; and growth characteristics by cell cycle analysis, cell growth, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide metabolic assays. These assays were also performed after transfection with a dominant negative (DN) BMPR1A construct. In SMAD4-null SW480 cells, we examined BMP effects on cellular wound assays as well as BMP-induced transcription in the presence of transfected SMAD4. We also determined the expression of BMPR1A, BMP ligands, and phospho-SMAD1 in primary human colon cancer specimens. We found intact BMP signaling and modest growth suppression in HCT116 and two derivative cell lines and, surprisingly, growth suppression in SMAD4-null SW480 cells. BMP-induced SMAD signaling and BMPR1A-mediated growth suppression were reversed with DN BMPR1A transfection. BMP2 slowed wound closure, and transfection of SMAD4 into SW480 cells did not change BMP-specific transcriptional activity over controls due to receptor stimulation by endogenously produced ligand. We found no cell cycle alterations with BMP treatment in the HCT116 and derivative cell lines, but there was an increased G1 fraction in SW480 cells that was not due to increased p21 transcription. In human colon cancer specimens, BMP2 and BMP7 ligands, BMPRIA, and phospho-SMAD1 were expressed. In conclusion, BMP signaling is intact and growth suppressive in human colon cancer cells. In addition to SMADs, BMP may utilize SMAD4-independent pathways for growth suppression in colon cancers.

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Liu, Zhirong, Yuehong Zhang, Jun Xie, Caiping Li, Xiaoxia Wang, Jinyan Shen, Yiqiang Zhang, Shiyu Wang, and Niuliang Cheng. "Regenerating Gene 1B Silencing Inhibits Colon Cancer Cell HCT116 Proliferation and Invasion." International Journal of Biological Markers 30, no. 2 (April 2015): 217–25. http://dx.doi.org/10.5301/jbm.5000133.

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Background The human regenerating gene 1B ( REG1B) is found to be frequently up-regulated in many types of human tumors. It is unclear whether REG1B expression may have therapeutic value in colorectal carcinoma. Additionally, how REG1B is associated with the clinical features of colorectal carcinoma is not known. To investigate the relationship between REG1B and colorectal cancer, we analyzed REG1B expression in clinical specimens and cell lines and the effect of down-regulation of REG1B by short hairpin RNA (shRNA) in HCT116 cells. Methods Paraffin-embedded specimens from 30 pairs of colorectal cancer tissues and adjacent colon tissues were used to investigate the expression of REG1B by immunohistochemistry. We also examined whether REG1B itself may be related to cell proliferation, cell cycle arrest, apoptosis, migration and invasion in colon cancer HCT116 cells. Results Our results showed that REG1B was highly expressed in colorectal carcinoma and was significantly associated with cell differentiation status. The results also illustrated that REG1B silencing with shRNA inhibited cell proliferation, migration and invasion but did not induce apoptosis. Furthermore, down-regulation of REG1B induces G1-phase cell cycle arrest in colon cancer cells. Conclusions Knockdown of REG1B can inhibit cell proliferation, migration and invasion. It may act by a mechanism regulating cell cycle progression. Thus, REG1B may be a novel candidate therapeutic target for colorectal cancer.

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Song, Xuemin, Dongming Luo, Qian Zhong, Ke Wei, Yangyang Tang, Dongbo Wu, Junyi Xu, and Pengcheng Yu. "Effect of Targeting Leucine-Zipper-Like Transcription Regulator 1 Gene on Colon Cancer Cells." Journal of Biomaterials and Tissue Engineering 11, no. 8 (August 1, 2021): 1588–94. http://dx.doi.org/10.1166/jbt.2021.2727.

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LZTR1 is associated with several diseases, including liver cancer, childhood cancer, and schwannomas. However, LZTR1’s role in colon cancer and its mechanism of action have not been reported. The colon cancer tissues and adjacent tissues were collected to measure the expression of LZTR1 by Real time PCR. Colon cancer SW620 cell lines were cultured and randomly divided into control group and LZTR1 group followed by analysis of LZTR1 expression by real time PCR, cell proliferation by MTT assay, Caspase3 activity, Bcl-2 and Bax level by Real time PCR, cell invasion by Transwell chamber; NF-κB/VEGF expression by Western blot. LZTR1 expression was significantly reduced in colon cancer tissues compared to adjacent tissues (P <0.05) and negatively correlated with colon cancer TNM stage, tumor size, and lymph node metastasis, and positively associated with tumor differentiation (P <0.05). LZTR1 plasmid transfection into SW620 cells can significantly up-regulate LZTR1, inhibit tumor cell proliferation and invasion, increase Caspase 3 activity and Bax level, downregulate Bcl-2, NF-κB and VEGF (P <0.05). LZTR1 expression is reduced in colon cancer tissues, which is related to its clinicopathological characteristics. Up-regulation of LZTR1 can regulate apoptosis and inhibit tumor proliferation and invasion by regulating NF-κB/VEGF signaling pathway.

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Jassbi, Amir Reza, Marzieh Vafapour, Ardeshir Shokrollahi, Omidreza Firuzi, Mehdi Zare, Jima N. Chandran, Bernd Schneider, and Ian T. Baldwin. "Cytotoxic Activity of Two Cembranoid Diterpenes from Nicotiana Sylvestris Against Three Human Cancer Cell Lines." Open Bioactive Compounds Journal 5, no. 1 (September 21, 2017): 1–8. http://dx.doi.org/10.2174/1874847301705010001.

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Background: Two cembranoid diterpenes, [(1S, 2E, 4R, 6R, 7E, 11E)-2, 7, 11-cembratriene-4, 6-diol] (1) and its epimer [(1S, 2E, 4S, 6R,7E,11E)-2, 7, 11-cembratriene-4, 6-diol] (2) were isolated from surface dichloromethane washings and chloroform extract of Nicotiana sylvestris leaves. Methods: The compounds were purified using silica gel column- thin layer- and flash column chromatography methods. The structures of the isolated compounds were elucidated using spectroscopic analysis and their 1H and 13C NMR spectroscopic data were compared with those of authentic samples reported in the literature. The cytotoxic activity of 1 and 2 against three human cancer cell lines, including LS180 (human colon adenocarcinoma), MCF-7 (human breast adenocarcinoma) and MOLT-4 (human lymphoblastic leukemia) were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric bioassay. Results: The IC50 values of compounds 1 and 2 were calculated to be between (28.4±3.7 up to 44.0±6.4 µM) (mean±S.E.M.) for the above mentioned cell lines.

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Guo, Yafei, Jiuling Li, Yuqi Liu, Yongping Ma, Huilin Cheng, Bo Yang, Dandan Liu, and Rui Yang. "Inclusion complexes of anhydrolycorine with cyclodextrins: preparation, characterization, and anticancer activity." Canadian Journal of Chemistry 94, no. 6 (June 2016): 575–82. http://dx.doi.org/10.1139/cjc-2015-0462.

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This article describes the preparation of a series of inclusion complexes of anhydrolycorine with three cyclodextrins (CDs), namely β-CD, γ-CD, and 2-hydroxypropyl-β-cyclodextrin (HP-β-CD), and their successful characterization through UV, TG, DSC, XRD, SEM, 1H NMR, and 2D NMR spectroscopies. The results demonstrated that the water solubility of anhydrolycorine increased notably by about 23–42 times after the inclusion complexation with these CDs. Furthermore, preliminary in vitro cytotoxicity experiments on human colon cancer cell lines HT-29, SW480, HCT116, and DLD-1 were also performed, and the complexes showed remarkable anticancer activity against HT-29, SW480, and HCT116. These results suggested that the inclusion complexes would be potentially useful for applications for human colon cancer chemotherapy.

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Haque, Rosenani A., Siti Fatimah Nasri, Muhammad Adnan Iqbal, Sawsan S. Al-Rawi, Seyedeh Fatemeh Jafari, Mohamed B. Khadeer Ahamed, and A. M. S. Abdul Majid. "Synthesis, Characterization, and Crystal Structures of Bis-Imidazolium Salts and Respective Dinuclear Ag(I)N-Heterocyclic Carbene Complexes:In VitroAnticancer Studies against “Human Colon Cancer” and “Breast Cancer”." Journal of Chemistry 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/804683.

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This paper describes synthesis, characterization (NMR, FT-IR, microanalysis, and X-ray crystallography),in vitroanticancer activity ofortho/para-xylyl linked bis-imidazolium salts (4-5) and respective dinuclear Ag(I)N-heterocyclic carbene (NHC) complexes (6-7). All the compounds were tested for their cytotoxicity against human colorectal cancer (HCT 116) and breast cancer (MCF-7) cell lines. According to cell viability measurements using MTT assay, all the complexes (6-7) showed a dose-dependent cytotoxic activity against both the cell lines, whereas respective salts (4-5) proved to be inactive. The complexes (6-7) demonstrated significant activity with IC50values range 5.6–20.3 μM for HCT 116 and 1.12–6.38 μM for MCF-7. 5-Fluorouracil was used as standard drug (IC50= 5.9 μM) for HCT 116, whereas tamoxifen was used as standard drug for MCF-7 (IC50= 14 μM) cell line.

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Hu, Shuiqing, Yan Fang, Xiang Chen, Tianlei Cheng, Miaoqing Zhao, Mingjian Du, Tuo Li, et al. "cGAS restricts colon cancer development by protecting intestinal barrier integrity." Proceedings of the National Academy of Sciences 118, no. 23 (June 1, 2021): e2105747118. http://dx.doi.org/10.1073/pnas.2105747118.

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The DNA-sensing enzyme cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) regulates inflammation and immune defense against pathogens and malignant cells. Although cGAS has been shown to exert antitumor effects in several mouse models harboring transplanted tumor cell lines, its role in tumors arising from endogenous tissues remains unknown. Here, we show that deletion of cGAS in mice exacerbated chemical-induced colitis and colitis-associated colon cancer (CAC). Interestingly, mice lacking cGAS were more susceptible to CAC than those lacking stimulator of interferon genes (STING) or type I interferon receptor under the same conditions. cGAS but not STING is highly expressed in intestinal stem cells. cGAS deficiency led to intestinal stem cell loss and compromised intestinal barrier integrity upon dextran sodium sulfate-induced acute injury. Loss of cGAS exacerbated inflammation, led to activation of STAT3, and accelerated proliferation of intestinal epithelial cells during CAC development. Mice lacking cGAS also accumulated myeloid-derived suppressive cells within the tumor, displayed enhanced Th17 differentiation, but reduced interleukin (IL)-10 production. These results indicate that cGAS plays an important role in controlling CAC development by defending the integrity of the intestinal mucosa.

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Erickson-Miller, Connie L., Antony Chadderton, Anna Gibbard, Jennifer Kirchner, Kodandaram Pillarisetti, Katherine Baker, Lini Pandite, et al. "Thrombopoietin Receptor Levels in Tumor Cell Lines and Primary Tumors." Journal of Oncology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/135354.

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Thrombopoietin (TPO) receptor agonists represent a new approach for the treatment of thrombocytopenia, which may develop as a consequence of immune thrombocytopenia, chemotherapy treatment, chronic hepatitis C infection, or myelodysplastic syndromes. There are concerns that use of certain growth factors can hasten disease progression in some types of hematologic malignancies and solid tumors. In this study, expression ofMPL(TPO-R) mRNA was examined in tumor cell lines, patient tumor samples (renal cell carcinoma, prostatic carcinoma, soft tissue and bony/cartilage sarcoma, colon cancer, and lymphoma), and normal tissues using microarray analysis and qRT-PCR.MPLmRNA is expressed at very low or undetectable levels compared with erythropoietin receptor (EPOR), human epidermal growth factor (ERBB2; HER2), and insulin-like growth factor-1 receptor (IGF1R) in these patient samples. These data suggest TPO-R agonists will likely preferentially stimulate proliferation and differentiation of cells of megakaryocytic lineage, potentially demonstrating their utility for correcting thrombocytopenia in clinical settings.

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Filip, Patrick, Roland W. S. Weber, Olov Sterner, and Timm Anke. "Hormonemate, a New Cytotoxic and Apoptosis-Inducing Compound from the Endophytic Fungus Hormonema dematioides. I. Identification of the Producing Strain, and Isolation and Biological Properties of Hormonemate." Zeitschrift für Naturforschung C 58, no. 7-8 (August 1, 2003): 547–52. http://dx.doi.org/10.1515/znc-2003-7-817.

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Abstract In a search for new fungal compounds inducing apoptosis of the colon cancer derived cell line COLO-320, hormonemate (1) was purified from fermentations of an endophytic fungus isolated from living needles of a Pinus species. The producing strain was identified as Hormonema dematioides by microscopy and ITS rDNA sequence analysis. The structure of hormonemate was determined by spectroscopic methods. The compound exhibited cytotoxic effects against the human colon tumor cell lines COLO-320, DLD-1 and HT-29 as well as five other human cell lines (HL-60, JURKAT, HEP-G2, MCF-7, HeLa S3). It also induced apoptosis in COLO-320 cells as detected by a caspase-activity assay and morphological changes, and it triggered morphological and physiological differentiation of HL-60 cells into granulocytes, which subsequently died by apoptosis.

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Choi, P. M., K. M. Tchou-Wong, and I. B. Weinstein. "Overexpression of protein kinase C in HT29 colon cancer cells causes growth inhibition and tumor suppression." Molecular and Cellular Biology 10, no. 9 (September 1990): 4650–57. http://dx.doi.org/10.1128/mcb.10.9.4650-4657.1990.

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By using a retrovirus-derived vector system, we generated derivatives of the human colon cancer cell line HT29 that stably overexpress a full-length cDNA encoding the beta 1 isoform of rat protein kinase C (PKC). Two of these cell lines, PKC6 and PKC7, displayed an 11- to 15-fold increase in PKC activity when compared with the C1 control cell line that carries the vector lacking the PKC cDNA insert. Both of the overexpresser cell lines exhibited striking alterations in morphology when exposed to the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Following exposure to TPA, PKC6 and PKC7 cells displayed increased doubling time, decreased saturation density, and loss of anchorage-independent growth in soft agar; but these effects were not seen with the C1 cells. Also, in contrast to the control cells, the PKC-overproducing cells failed to display evidence of differentiation, as measured by alkaline phosphatase activity, when exposed to sodium butyrate. In addition, the PKC-overexpresser cells displayed decreased tumorigenicity in nude mice, even in the absence of treatment with TPA. These results provide the first direct evidence that PKC can inhibit tumor cell growth. Thus, in some tumors, PKC might act as a growth-suppressor gene.

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Khusnutdinova, Elmira F., Alexander I. Poptsov, and Oxana B. Kazakova. "Synthesis and Cytotoxic Potential of 3-oxo-19β-Trifluoroacetoxy-18αH-oleane-28-oic Acid." Molbank 2021, no. 2 (June 1, 2021): M1222. http://dx.doi.org/10.3390/m1222.

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Trifluoroacetic acid-promoted Wagner-Meerwein rearrangement of betulonic acid carboxamide led to the formation of the expected 19β,28-lactam along with a new germanicane-type 3-oxo-19β-trifluoroacetoxy-18αH-oleane-28-oic acid. The structure of this triterpenoid was confirmed by 2D NMR analyses. A primary evaluation of biological potency revealed an anticancer activity with GI50 < 5 μM against leukemia, colon cancer, breast cancer, and prostate cancer cell lines, while the parent compounds were not active.

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33

Choi, P. M., K. M. Tchou-Wong, and I. B. Weinstein. "Overexpression of protein kinase C in HT29 colon cancer cells causes growth inhibition and tumor suppression." Molecular and Cellular Biology 10, no. 9 (September 1990): 4650–57. http://dx.doi.org/10.1128/mcb.10.9.4650.

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By using a retrovirus-derived vector system, we generated derivatives of the human colon cancer cell line HT29 that stably overexpress a full-length cDNA encoding the beta 1 isoform of rat protein kinase C (PKC). Two of these cell lines, PKC6 and PKC7, displayed an 11- to 15-fold increase in PKC activity when compared with the C1 control cell line that carries the vector lacking the PKC cDNA insert. Both of the overexpresser cell lines exhibited striking alterations in morphology when exposed to the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Following exposure to TPA, PKC6 and PKC7 cells displayed increased doubling time, decreased saturation density, and loss of anchorage-independent growth in soft agar; but these effects were not seen with the C1 cells. Also, in contrast to the control cells, the PKC-overproducing cells failed to display evidence of differentiation, as measured by alkaline phosphatase activity, when exposed to sodium butyrate. In addition, the PKC-overexpresser cells displayed decreased tumorigenicity in nude mice, even in the absence of treatment with TPA. These results provide the first direct evidence that PKC can inhibit tumor cell growth. Thus, in some tumors, PKC might act as a growth-suppressor gene.

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Berenson, Charles S., Melissa A. Patterson, Jehad A. Miqdadi, and Peter Lance. "n-Butyrate Mediation of Ganglioside Expression of Human and Murine Cancer Cells Demonstrates Relative Cell Specificity." Clinical Science 88, no. 4 (April 1, 1995): 491–99. http://dx.doi.org/10.1042/cs0880491.

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1. n-Butyrate, a short chain fatty acid produced by colonic fermentation, induces differentiation in human neoplastic cell lines, and reduces expression in vitro of a sialyltransferase that glycosylates N-linked glycoproteins in hepatoblastoma cells. Gangliosides are amphipathic, sialylated glycosphingolipids that undergo profound changes in many transformed cells and may protect neoplastic cells from host immune surveillance. Colonic mucosal cells are exposed to luminal short-chain fatty acid concentrations of up to 80 mmol/l, and there is some evidence that short-chain fatty acids may alter ganglioside expression in colon cancer cells. 2. Because of the importance of gangliosides in cancer pathogenesis, we investigated the effects of n-butyrate on ganglioside expression of colonic (human and murine) and non-colonic cancer cells. 3. Three separate colon cancer cell lines (LS174T, T84 and MCA-38), when butyrate treated, demonstrated striking amplification of specific individual gangliosides. However, the total lipid-bound sialic acid content of gangliosides of butyrate-treated LS174T cells diminished. In contrast to earlier reports, n-butyrate did not mediate expression of all gangliosides and specifically did not mediate expression of GM3. This effect persisted even after removal of butyrate. 4. In contrast, exposure of extracolonic cells to butyrate, including cervical cancer (HeLa) and laryngeal cancer (HEp-2) cell lines in this study and hepatoblastoma cells (Hep G2) in our previous work, caused no detectable changes in ganglioside expression. 5. In conclusion, our results indicate a relative tissue specificity of butyrate-mediated alterations in ganglioside expression that is not universal but is limited to specific gangliosides.

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Caporali, Sabrina, Cosimo Calabrese, Marilena Minieri, Massimo Pieri, Umberto Tarantino, Mario Marini, Stefano D’Ottavio, et al. "The miR-133a, TPM4 and TAp63γ Role in Myocyte Differentiation Microfilament Remodelling and Colon Cancer Progression." International Journal of Molecular Sciences 22, no. 18 (September 10, 2021): 9818. http://dx.doi.org/10.3390/ijms22189818.

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MicroRNAs (miRNAs) play an essential role in the regulation of a number of physiological functions. miR-133a and other muscular miRs (myomiRs) play a key role in muscle cell growth and in some type of cancers. Here, we show that miR133a is upregulated in individuals that undertake physical exercise. We used a skeletal muscle differentiation model to dissect miR-133a’s role and to identify new targets, identifying Tropomyosin-4 (TPM4). This protein is expressed during muscle differentiation, but importantly it is an essential component of microfilament cytoskeleton and stress fibres formation. The microfilament scaffold remodelling is an essential step in cell transformation and tumour progression. Using the muscle system, we obtained valuable information about the microfilament proteins, and the knowledge on these molecular players can be transferred to the cytoskeleton rearrangement observed in cancer cells. Further investigations showed a role of TPM4 in cancer physiology, specifically, we found that miR-133a downregulation leads to TPM4 upregulation in colon carcinoma (CRC), and this correlates with a lower patient survival. At molecular level, we demonstrated in myocyte differentiation that TPM4 is positively regulated by the TA isoform of the p63 transcription factor. In muscles, miR-133a generates a myogenic stimulus, reducing the differentiation by downregulating TPM4. In this system, miR-133a counteracts the differentiative TAp63 activity. Interestingly, in CRC cell lines and in patient biopsies, miR-133a is able to regulate TPM4 activity, while TAp63 is not active. The downregulation of the miR leads to TPM4 overexpression, this modifies the architecture of the cell cytoskeleton contributing to increase the invasiveness of the tumour and associating with a poor prognosis. These results add data to the interesting question about the link between physical activity, muscle physiology and protection against colorectal cancer. The two phenomena have in common the cytoskeleton remodelling, due to the TPM4 activity, that is involved in stress fibres formation.

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Jęśkowiak, Izabela, Stanisław Ryng, Marta Świtalska, Joanna Wietrzyk, Iwona Bryndal, Tadeusz Lis, and Marcin Mączyński. "The N’-Substituted Derivatives of 5-Chloro-3-Methylisothiazole-4-Carboxylic Acid Hydrazide with Antiproliferative Activity." Molecules 25, no. 1 (December 25, 2019): 88. http://dx.doi.org/10.3390/molecules25010088.

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Thanks to the progress in oncology, pharmacological treatment of cancer is gaining in importance and in the near future anti-cancer chemotherapeutics are expected to be the main method of treatment for cancer diseases. What is more, the search for new anti-cancer compounds with the desired application properties is constantly underway. As a result of designed syntheses, we obtained some new N’-substituted 5-chloro-3-methylisothiazole-4-carboxylic acid hydrazide derivatives with anticancer activity. The structure of new compounds was determined by mass spectrometry (MS), elemental analysis, proton nuclear magnetic resonance spectroscopy (1H-NMR), carbon nuclear magnetic resonance spectroscopy (13C-NMR), 1H-13C NMR correlations and infrared spectroscopy (IR). Moreover, the structures of the compounds were confirmed by crystallographic examination. The antiproliferative MTT tests for 11 prepared compounds was conducted towards human biphenotypic B cell myelomonocytic leukemia MV4-11. SRB test was used to examine their potential anticancer activity towards human colon adenocarcinoma cell lines sensitive LoVo, resistant to doxorubicin LoVo/DX, breast adenocarcinoma MCF-7 and normal non-tumorigenic epithelial cell line derived from mammary gland MCF-10A. The most active compound was 5-chloro-3-methyl-N′-[(1E,2E)-(3-phenyloprop-2-en-1-ylidene]isothiazole-4-carbohydrazide, which showed the highest antiproliferative activity against all tested cell lines.

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Abdel-Sattar, Essam, Azza R. Abdel Monem, Shahira M. Ezzat, Ali M. El-Halawany, and Samar M. Mouneir. "Chemical and Biological Investigation of Araucaria heterophylla Salisb. Resin." Zeitschrift für Naturforschung C 64, no. 11-12 (December 1, 2009): 819–23. http://dx.doi.org/10.1515/znc-2009-11-1211.

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Three labdane diterpenes, namely labda-8(17),14-diene, 13-epicupressic acid, and 13-Oacetyl- 13-epicupressic acid, were isolated from the resin collected from stem exudates of Araucaria heterophylla Salisb. (Araucariaceae). The isolated compounds were identified using different spectroscopic methods (1H NMR, 13C NMR, HMQC, HMBC and COSY). The resin extract showed antiulcerogenic activity against ethanol-induced stomach ulcers in Sprauge Dawely rats using ranitidine as standard. In addition, the resin and the isolated compounds showed variable cytotoxic activities against breast (MCF7) and colon (HCT116) cancer cell lines.

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Belal, Amany. "Pyrrolizines as Potential Anticancer Agents: Design, Synthesis, Caspase-3 activation and Micronucleus (MN) Induction." Anti-Cancer Agents in Medicinal Chemistry 18, no. 15 (February 28, 2019): 2124–30. http://dx.doi.org/10.2174/1871520618666180409155520.

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Background: For further exploration of the promising pyrrolizine scaffold and in continuation of our previous work, that proved the potential anticancer activity of the hit compound I, a new series of pyrrolizines 2-5 and 7-9 were designed and synthesized. Methods: Structures of the new compounds were confirmed by IR, 1H-NMR, 13C-NMR and elemental analysis. Antitumor activity for the prepared compounds against human breast adenocarcinoma (MCF-7), liver (HEPG2) and colon (HCT116) cancer cell lines was evaluated using SRB assay method. Result: Compounds 2, 3 and 5 were the most potent on colon cancer cells, their IC50 values were less than 5 µM. Compounds 2, 3 and 8 were the most potent on liver cancer cells, their IC50 values were less than 10 µM. As for MCF7, compounds 2, 7, 8 and 9 were the most active with IC50 values less than 10 µM. We can conclude that combining pyrrolizine scaffold with urea gave abroad spectrum anticancer agent 2 against the three tested cell lines. Micronucleus assays showed that compounds 2, 3, 8 are mutagenic and can induce apoptosis. In addition, caspase-3 activation was evaluated and compound 2 showed increase in the level of caspase-3 (9 folds) followed by 3 (8.28 folds) then 8 (7.89 folds). Conclusion: The obtained results encourage considering these three compounds as novel anticancer prototypes.

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CAPON, Calliope, Emmanuel MAES, Jean-Claude MICHALSKI, Hakon LEFFLER, and Young S. KIM. "Sda-antigen-like structures carried on core 3 are prominent features of glycans from the mucin of normal human descending colon." Biochemical Journal 358, no. 3 (September 10, 2001): 657–64. http://dx.doi.org/10.1042/bj3580657.

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This paper describes structural characterization by NMR, MS and degradative studies of mucin glycans from normal human descending colon obtained freshly at autopsy. The saccharides were mainly based on core 3 (GlcNAcβ1-3GalNAc). Among the terminal saccharide determinants Sda/Cad-antigen-like structures were prominent, and Lewis x, sialyl Lewis x and sulphated Lewis x were found as minor components, whereas blood group H and A antigenic determinants were absent. The saccharides were markedly different from those of mucins from colon cancers or colon cancer cell lines analysed so far, in which cores 1 and 2 are prominent features, and in which various other terminal determinants have been found, but not Sda/Cad.

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Holst, Stephanie, Jennifer Wilding, Kamila Koprowska, Yoann Rombouts, and Manfred Wuhrer. "N-Glycomic and Transcriptomic Changes Associated with CDX1 mRNA Expression in Colorectal Cancer Cell Lines." Cells 8, no. 3 (March 22, 2019): 273. http://dx.doi.org/10.3390/cells8030273.

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The caudal-related homeobox protein 1 (CDX1) is a transcription factor, which is important in the development, differentiation, and homeostasis of the gut. Although the involvement of CDX genes in the regulation of the expression levels of a few glycosyltransferases has been shown, associations between glycosylation phenotypes and CDX1 mRNA expression have hitherto not been well studied. Triggered by our previous study, we here characterized the N-glycomic phenotype of 16 colon cancer cell lines, selected for their differential CDX1 mRNA expression levels. We found that high CDX1 mRNA expression associated with a higher degree of multi-fucosylation on N-glycans, which is in line with our previous results and was supported by up-regulated gene expression of fucosyltransferases involved in antenna fucosylation. Interestingly, hepatocyte nuclear factors (HNF)4A and HNF1A were, among others, positively associated with high CDX1 mRNA expression and have been previously proven to regulate antenna fucosylation. Besides fucosylation, we found that high CDX1 mRNA expression in cancer cell lines also associated with low levels of sialylation and galactosylation and high levels of bisection on N-glycans. Altogether, our data highlight a possible role of CDX1 in altering the N-glycosylation of colorectal cancer cells, which is a hallmark of tumor development.

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Nakajima, E., B. Helfrich, D. Chan, Z. Zhang, F. R. Hirsch, V. Chen, D. Ma, and P. A. Bunn. "Enzastaurin a protein kinase Cbeta-selective inhibitor, inhibits the growth of SCLC and NSCLC cell lines." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 13138. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13138.

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13138 Background: PKCβ is a member of the PKC family of serine-threonine protein kinases involved in tumor cell proliferation and apoptosis. Inhibition of PKCs induced differentiation and enhanced chemotherapy. PKCβ activation is required for tumor-induced angiogenesis. The PKCβ-selective inhibitor enzastaurin, originally developed as an antiangiogenic agent, inhibited tumor cell proliferation in prostate, colon and glioblastoma cell lines in vitro. In NSCLC lines, enhanced phosphorylation and altered PKC expression was demonstrated. In SCLC lines specific PKC isoforms were associated with cisplatin resistance. Methods: The growth inhibitory effects of enzastaruin were evaluated by 6-day MTT assays; the cell cycle effects by FACS analysis; the effects on downstream phophorylated signaling molecules by western blotting. Results: Enzastaurin inhibited the growth of 11 SCLC lines (IC50s 3–10 μM) and 4 NSCLC cell lines (IC50s 3–10 μM). An increase of 7–31% of cells in the G2/M phase of the cell cycle compared to untreated control was observed following 48 hour exposure to the IC50 dose of enzastaurin in both SCLC and NSCLC cell lines. PKCβ has been shown to phosphorylate both GSK3β and Akt. A 24-hour IC50 enzastaurin exposure significantly reduced phosphorylation of GSK3β (Ser9) in both SCLC and NSCLC lines. No changes were observed in phospho-AKT (Thr308) in either SCLC or NSCLC cell lines. Phospho-ribosomal protein S6 (Ser240/244) was also reduced in both SCLC and NSCLC cell lines. Potential synergy was studied between enzastaurin and pemetrexed in SCLC and NSCLC lines and the results were analyzed using the Calcusyn Program by Chou and Talalay. Synergistic (CI <1) to additive interactions were observed between pemetrexed (IC20–70) and enzastaurin (≤ IC50) in both SCLC lines (N = 3) and NSCLC lines (N = 2). Conclusions: We conclude that enzastaruin produces in vitro growth inhibition of SCLC and NSCLC cell lines through inhibition of GSK3β ser9 phosphorylation and has synergistic growth inhibition with pemetrexed. [Table: see text]

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Alex, A. Renjith, and K. Ilango. "IN VITRO CYTOTOXIC ACTIVITY OF ISOLATED COMPOUNDS FROM VIBURNUM PUNCTATUM BUCH-HAM EX D. DON." International Journal of Current Pharmaceutical Research 9, no. 1 (December 31, 2016): 85. http://dx.doi.org/10.22159/ijcpr.2017v9i1.16622.

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Objective: The main aim of the study was to screen the isolated compounds of Viburnum Punctatum for its in vitro anticancer activity and its percentage viability against HCT 15 (Human Colon Cancer Cells) Cell lines.Methods: Pet ether, Chloroform, Methanol and Aqueous extracts was prepared and assayed for the presence of phytochemicals. Two compounds were isolated from the methanol extract of Viburnum Punctatum by column chromatography such as ME1 (Quercetin) and ME2 (Kaemferol-3-glycoside) characterised by UV, IR, MS, 1H NMR and 13C NMR. The above isolated compounds were subjected to in vitro anticancer activity on HCT 15 cell lines was evaluated by Micro culture Tetrazolium (MTT) assay.Results: ME1 showed significant cytotoxic activity than the ME2 on HCT 15 cells with a percentage viability of 54.60 and 67.18 in the concentration of 10µg/ml and 50µg/ml respectively.Conclusion: On the basis of obtained results, ME1 and ME2 isolated from a methanolic extract of Viburnum Punctatum represent a new group of cytotoxic against HCT 15 Cell lines.

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De Araújo, Mônica Regina Silva, João Carlos Da Costa Assunção, Ivana Nogueira Fernandes Dantas, Letícia Veras Costa-Lotufo, and Francisco José Queiroz Monte. "Chemical Constituents of Ximenia Americana." Natural Product Communications 3, no. 6 (June 2008): 1934578X0800300. http://dx.doi.org/10.1177/1934578x0800300605.

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Two steroids (1 and 2), five pentacyclic triperpenoids (3–7) and a new furanosesquiterpene (8) were isolated from the stems of Ximenia americana, family Olacaceae. The structures of the compounds were established by spectral data; two-dimensional NMR spectroscopy has been used to assign all 1H and 13C chemical shifts of 8. Compound 8 did not inhibit the growth of HL-60 (human leukemia), HTC-8 (human colon), and MDA-MB-435 (human breast cancer) cell lines.

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Zhang, Hanyu, Mingxing Li, Parham Jabbarzadeh Kaboli, Huijiao Ji, Fukuan Du, Xu Wu, Yueshui Zhao, et al. "Identification of cluster of differentiation molecule-associated microRNAs as potential therapeutic targets for gastrointestinal cancer immunotherapy." International Journal of Biological Markers 36, no. 2 (March 31, 2021): 22–32. http://dx.doi.org/10.1177/17246008211005473.

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Background: Cluster of differentiation molecules are markers of immune cells that have been identified as a potential immunotherapeutic target for cancer treatment. MicroRNAs are small non-coding RNAs that act as tumor suppressors or oncogenes whose importance in diagnosis, prognosis, and treatment of gastric and colorectal cancers has been widely reported. However, their association with cluster of differentiation molecules in gastrointestinal cancers has not been well studied. Therefore, our study aimed to analyze the relationship between microRNAs and cluster of differentiation molecules in gastrointestinal cancers, and to identify cluster of differentiation molecule-associated microRNAs as prognostic biomarkers for gastrointestinal cancer patients. Methods: Targetscan, Starbase, DIANA microT, and miRDB were used to investigate microRNA profiles that might be correlated with cluster of differentiation molecules in gastrointestinal cancers. Moreover, The Cancer Genome Atlas data analysis was used to investigate the association between cluster of differentiation molecules and microRNA expression in patients with gastric, colon, rectal, pancreatic, and esophageal cancers. The Kaplan–Meier plotter was used to identify the association between overall survival and cluster of differentiation molecule-associated microRNA expression in gastrointestinal cancer patients. Results: miR-200a, miR-559, and miR-1236 were negatively associated with CD86, CD81, and CD160, respectively, in almost all types of gastrointestinal cancers, which were further verified in the in vitro studies by transfecting microRNA mimics in gastric cancer, colon cancer, pancreatic, and esophageal cell lines. Conclusion: Our study showed that miR-200a, miR-1236, and miR-559 are identified as cluster of differentiation-associated microRNAs in gastrointestinal cancers, providing a novel perspective to identify new therapeutic targets for cancer immunotherapy in gastrointestinal cancer patients.

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Graziani, Vittoria, Assunta Esposito, Monica Scognamiglio, Angela Chambery, Rosita Russo, Fortunato Ciardiello, Teresa Troiani, Nicoletta Potenza, Antonio Fiorentino, and Brigida D’Abrosca. "Spectroscopic Characterization and Cytotoxicity Assessment towards Human Colon Cancer Cell Lines of Acylated Cycloartane Glycosides from Astragalus boeticus L." Molecules 24, no. 9 (May 3, 2019): 1725. http://dx.doi.org/10.3390/molecules24091725.

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In several European countries, especially in Sweden, the seeds of the species Astragalus boeticus L. were widely used as coffee substitutes during the 19th century. Nonetheless, data regarding the phytochemistry and the pharmacological properties of this species are currently extremely limited. Conversely, other species belonging to the Astragalus genus have already been extensively investigated, as they were used for millennia for treating various diseases, including cancer. The current work was addressed to characterize cycloartane glycosides from A. boeticus, and to evaluate their cytotoxicity towards human colorectal cancer (CRC) cell lines. The isolation of the metabolites was performed by using different chromatographic techniques, while their chemical structures were elucidated by nuclear magnetic resonance (NMR) (1D and 2D techniques) and electrospray-ionization quadrupole time-of-flight (ESI-QTOF) mass spectrometry. The cytotoxic assessment was performed in vitro by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays in Caco-2, HT-29 and HCT-116 CRC cells. As a result, the targeted phytochemical study of A. boeticus enabled the isolation of three new cycloartane glycosides, 6-O-acetyl-3-O-(4-O-malonyl)-β-d-xylopyranosylcycloastragenol (1), 3-O-(4-O-malonyl)-β-d-xylopyranosylcycloastragenol (2), 6-O-acetyl-25-O-β-d-glucopyranosyl-3-O-β-d-xylopyranosylcycloastragenol (3) along with two known compounds, 6-O-acetyl-3-O-β-d-xylopyranosylcycloastragenol (4) and 3-O-β-d-xylopyranosylcycloastragenol (5). Importantly, this work demonstrated that the acetylated cycloartane glycosides 1 and 4 might preferentially inhibit cell growth in the CRC cell model resistant to epidermal growth factor receptor (EGFR) inhibitors.

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Deng, Y., L. Wang, Q. Tian, C. Miller, T. Lin, A. J. Chien, C. M. Ulrich, W. M. Grady, C. A. Blau, and E. H. Lin. "Regulation of expression of cd133, a colon cancer stem cell marker and other stemness genes/pathways, by celecoxib: Clues from clinical observations." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e15065-e15065. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e15065.

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e15065 Background: CD133 identifies intestinal stem cells and colon CSC, the putative culprit of cancer initiation, progression and resistance. Elevated CD133 levels at protein & mRNA levels predict poor outcomes in patients (pts) with colon cancer. Given that celecoxib reduces colon polyp and only maintenance capecitabine plus celecoxib lead to paradoxically high complete remission (CR) in colon cancer pts who had no resection or positive margin resection of metastases (ASCO 2007), we hypothesized that celecoxib could modulate CD133 and other stemness genes/signaling pathways. Methods: we studied the effects of celecoxib versus 5-FU on CD133, Wnt and other stemness genes/pathways using flow cytometry, immunoflurorescence, real time RT-PCR, western blot, TOP-Flash for Wnt, limiting dilution assay, and Affymetrix in colon cancer cell lines and primary colon cancer spheres. Results: Celecoxib or 5FU inhibited the growth of COX-2+ HT29 or COX-2- DLD1 that express CD133 at 80% and 30% respectively. Only celecoxib down-regulated CD133 expression at the mRNA, and protein levels in a dose and time dependent manner. This effect could not be rescued with PGE2 and may be due to Wnt inhibition. Microarray showed 4 folds down-regulation of CD133 and other stemness genes e.g. CD24, ABC transporters, and LGR4/5, findings of colon cancer sphere under differentiation. Celecoxib affected several key stem cells signaling pathway, restored RB and promote cell cycle progression (P < 0.05). In contrast, 5FU affected G2M transition but had no effects on stemness genes/pathways (p < 0.05). Celecoxib resulted in 6–10 folds reduction in colony size and number with 5.6–36 folds down-regulation of CD133 mRNA in primary colon cancer spheres. Pts with confirmed radiographic CR who had received >6 months of maintenance capecitabine and celecoxib reached 5-year survival > 90% comparable to pts who achieved pathological CR (12/19). Conclusions: Targeting colon CSC with capecitabine and celecoxib may lead to durable CR and survival and deserves further investigation. No significant financial relationships to disclose.

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Sameem, Bilqees, Ebrahim Saeedian Moghadam, Majid Darabi, Zahra Shahsavari, and Mohsen Amini. "Triarylpyrazole Derivatives as Potent Cytotoxic Agents; Synthesis and Bioactivity Evaluation “Pyrazole Derivatives as Anticancer Agent”." Drug Research 71, no. 07 (May 19, 2021): 388–94. http://dx.doi.org/10.1055/a-1498-1714.

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Abstract Background During the last recent years, several anti-cancer agents were introduced for the treatment of diverse kinds of cancer. Despite their potential in the treatment of cancer, drug resistance and adverse toxicity such as peripheral neuropathy are some of the negative criteria of anti-cancer agents and for this reason, the design and synthesis of new anti-cancer agents are important. Objective Design, synthesis, and anticancer activity evaluation of some pyrazole derivatives. Methods A series of Target compounds were prepared using multistep synthesis. Their cytotoxic activity against three different human cancer cell lines namely human colon carcinoma cells (HT-29), epithelial carcinoma cells (U-87MG), pancreatic cancerous cells (Panc-1) as well as AGO1522 normal cell line using in vitro 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was investigated. Results 1,3-Diaryl-5-(3,4,5-trimethoxyphenyl)-4,5-dihydro-1H-pyrazole and 1,3-Diaryl-5-(3,4,5-trimethoxyphenyl)- 1H-pyrazole were synthesized in good yields and their structure and purity were confirmed using 1H-NMR, 13C-NMR, and elemental analysis. Generally, the synthesized scaffolds exhibited good cytotoxicity against cancerous cell lines in comparison to the reference standard, paclitaxel. Compounds 3a and 3c, in Annexin V/ PI staining assay, exerted remarkable activity in apoptosis induction in HT-29 cell lines. Both of them also led to cell cycle arrest in the sub-G1 phase which is inconsistent with the results of apoptosis assay. Conclusion Concerning obtained results, it is interesting to synthesis more pyrazole derivatives as anticancer agents.

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Mihci-Gaidi, Ghezala, David Pertuit, Tomofumi Miyamoto, Jean-François Mirjolet, Olivier Duchamp, Anne-Claire Mitaine-Offer, and Marie-Aleth Lacaille-Dubois. "Triterpene Saponins from Cyclamen persicum." Natural Product Communications 5, no. 7 (July 2010): 1934578X1000500. http://dx.doi.org/10.1177/1934578x1000500707.

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A new triterpene saponin 3- O-β-D-glucopyranosyl-(1→4)-α-L-arabinopyranosyl-16α-hydroxy-13β,28-epoxy-oleanan-30-al (1), along with four known triterpene glycosides (2-5) were isolated from Cyclamen persicum. Their structures were characterized by a combination of 1D- and 2D-NMR (1H-1H COSY, TOCSY, NOESY, HSQC, and HMBC) and MS spectrocopic data. The cytotoxicity of compounds 2 and 4 was evaluated using two human colon cancer cell lines HT-29 and HCT 116.

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Alorfi, Hajer S., Mohamed A. Ghandourah, and Adnan J. Turki. "Cytotoxic effect of acetogenins and sesquiterpenes obtained from the Red alga Laurencia majuscula." Tropical Journal of Pharmaceutical Research 19, no. 3 (April 9, 2020): 583–86. http://dx.doi.org/10.4314/tjpr.v19i3.18.

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Purpose: To evaluate the cytotoxicity of n-hexane extract and its metabolites obtained from the red alga, Laurencia majuscula, against three cancer cell lines HCT-116 (colon cancer), PC-3 (prostate cancer) and HepG2 (liver cancer) cells; and to identify the phytochemical compound(s) involved. Methods: Solvent extraction, thin layer chromatography, aluminum oxide column chromatography, and preparative thin layer chromatography (PTLC) were employed for isolating pure compounds from nhexane extract of Laurencia majuscula. Nuclear magnetic resonance (NMR) and mass spectrometry (MS) measurements were used for structural elucidation of the compounds. The cytotoxicity of the nonpolar extract and isolated compounds were evaluated against HCT, PC-3, and HepG2 cells using MTT assay, relative to the standard cytotoxic drug (cisplatin). Results: Three sesquiterpenes (1, 2 and 8), and five acetogenins (3-7) were isolated from the n-hexane extract. The n-hexane extract showed higher potent cytotoxic effect than sesquiterpenes and the acetogenins (3-7). Conclusion: These results indicate that the n-hexane extract of Laurencia majuscula exerts significant cytotoxicity against HCT-116, PC-3 and HepG2 cell lines, thus suggesting that the plant extract may be effective chemotherapeutic agents for the management of colon, postrate and liver cancer. Keywords: Red Sea alga, Rhodomelaceae, Polyketides, Terpenes, Anticancer

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Elsayed, Shadia A., Ahmed M. El-Hendawy, Sahar I. Mostafa, Bertrand J. Jean-Claude, Margarita Todorova, and Ian S. Butler. "Antineoplastic Activity of New Transition Metal Complexes of 6-Methylpyridine-2-carbaldehyde-N(4)-ethylthiosemicarbazone: X-Ray Crystal Structures of [VO2(mpETSC)] and [Pt(mpETSC)Cl]." Bioinorganic Chemistry and Applications 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/149149.

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New complexes of dioxovanadium(V), zinc(II), ruthenium(II), palladium(II), and platinum(II) with 6-methylpyridine-2-carbaldehyde-N(4)-ethylthiosemicarbazone (HmpETSC) have been synthesized. The composition of these complexes is discussed on the basis of elemental analyses, IR, Raman, NMR (H1,C13, andP31), and electronic spectral data. The X-ray crystal structures of [VO2(mpETSC)] and [Pt(mpETSC)Cl] are also reported. The HmpETSC and its [Zn(HmpETSC)Cl2] and [Pd(mpETSC)Cl] complexes exhibit antineoplastic activity against colon cancer human cell lines (HCT 116).

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Journal articles on the topic 'Cancer, differentiation, NMR, colon cell lines'

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