Добірка наукової літератури з теми "A375 Melanoma cells"
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Статті в журналах з теми "A375 Melanoma cells"
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Chang, Meng-Ting, Jia-Hua Feng, Kyoko Nakagawa-Goto, Kuo-Hsiung Lee, and Lie-Fen Shyur. "Abstract PR05: Unique lipid metabolite profiling in BRAFV600E inhibitor drug-resistant melanoma and their potential as drug target." Cancer Research 80, no. 19_Supplement (October 1, 2020): PR05. http://dx.doi.org/10.1158/1538-7445.mel2019-pr05.
Повний текст джерелаАнотація:
Abstract Melanoma is the most life-threatening skin cancer in the world. Advanced melanoma is highly metastatic, commonly develops drug resistance, and causes low survival rate in patients. PLX4032 (vemurafenib), a BRAFV600E inhibitor, is used to treat patients with late-stage melanoma. It showed initial good clinical responses but relapsed due to acquired drug resistance in tumors. The mechanism of PLX4032-induced resistance in melanoma is not well characterized; in particular, whether PLX4032-induced drug resistance in BRAF mutant melanoma would alter lipid metabolism in cancer is not clear. Understanding the status and role of lipid mediators (oxylipins) in melanoma pathology may be crucial for developing effective approach to overcome drug resistance. Our laboratory has demonstrated that plant sesquiterpene lactone deoxyelephantopin (DET) and its novel derivative DETD-35 effectively suppressed human A375 BRAFV600E melanoma with acquired drug resistance to PLX4032 in vitro and in xenograft mice. In this study we aimed to identify potential biomarkers associated with the resistant melanoma cells (A375-R) in the context of bioactive lipid mediators and to investigate whether DETD-35/DET effects against drug-resistant melanoma are through regulating their dynamics and contents. MS-based metabolomics was used to comprehensively analyze the oxylipin profiles in A375 and A375-R cells, mouse A375/A375-R tumor tissues, and respective sera with vehicle, drug, or compound treatment. We observed that PLX4032-resistant A375R melanoma cells or tumors produce significant and higher amounts of CYP450 enzyme-derived oxylipins than the parental A375, which were decreased after DETD-35 or DET treatment. This study proposes a role of CYP450-derived oxylipins in PLX4032-resistant melanoma cells and its potential to be a drug target. This abstract is also being presented as Poster B03. Citation Format: Meng-Ting Chang, Jia-Hua Feng, Kyoko Nakagawa-Goto, Kuo-Hsiung Lee, Lie-Fen Shyur. Unique lipid metabolite profiling in BRAFV600E inhibitor drug-resistant melanoma and their potential as drug target [abstract]. In: Proceedings of the AACR Special Conference on Melanoma: From Biology to Target; 2019 Jan 15-18; Houston, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(19 Suppl):Abstract nr PR05.
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Haasler, Lisa, Arun Kumar Kondadi, Thanos Tsigaras, Claudia von Montfort, Peter Graf, Wilhelm Stahl, and Peter Brenneisen. "The BH3 mimetic (±) gossypol induces ROS-independent apoptosis and mitochondrial dysfunction in human A375 melanoma cells in vitro." Archives of Toxicology 95, no. 4 (February 1, 2021): 1349–65. http://dx.doi.org/10.1007/s00204-021-02987-4.
Повний текст джерелаАнотація:
AbstractA major challenge in current cancer therapy is still the treatment of metastatic melanomas of the skin. BH3 mimetics represent a novel group of substances inducing apoptosis. In this study, we investigated the cytotoxic effect of (±) gossypol (GP), a natural compound from cotton seed, on A375 melanoma cells and the underlying biochemical mechanisms. To prevent undesired side effects due to toxicity on normal (healthy) cells, concentrations only toxic for tumor cells have been elaborated. Viability assays were performed to determine the cytotoxicity of GP in A375 melanoma and normal (healthy) cells. For the majority of experiments, a concentration of 2.5 µM GP was used resulting in a ROS-independent but caspase-dependent cell death of A375 melanoma cells. At this level, GP was non-toxic for normal human epidermal melanocytes. GP has a very short half-life, however, it was demonstrated that only the “parent” compound and not decomposition products are responsible for the cytotoxic effect in A375 melanoma cells. GP significantly decreased mitochondrial membrane potential accompanied by a Drp1-dependent loss of mitochondrial integrity (fragmentation) in tumor cells. Taken together, GP induced a ROS-independent intrinsic apoptosis leading to the conclusion that within a specific concentration range, GP may work as effective anticancer drug without harmful side effects.
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Wu, Shih-Yen, Shih-Pin Huang, Yen-Chen Lo, Ren-Shyan Liu, Shyh-Jen Wang, Wuu-Jyh Lin, Chih-Chieh Shen, and Hsin-Ell Wang. "Synthesis and Preclinical Characterization of [18F]FPBZA: A Novel PET Probe for Melanoma." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/912498.
Повний текст джерелаАнотація:
Introduction. Benzamide can specifically bind to melanoma cells. A18F-labeled benzamide derivative, [18F]N-(2-diethylaminoethyl)-4-[2-(2-(2-fluoroethoxy) ethoxy)ethoxy]benzamide ([18F]FPBZA), was developed as a promising PET probe for primary and metastatic melanoma.Methods. [18F]FPBZA was synthesized via a one-step radiofluorination in this study. The specific uptake of [18F]FPBZA was studied in B16F0 melanoma cells, A375 amelanotic melanoma cells, and NB-DNJ-pretreated B16F0 melanoma cells. The biological characterization of [18F]FPBZA was performed on mice bearing B16F0 melanoma, A375 amelanotic melanoma, or inflammation lesion.Results. [18F]FPBZA can be prepared efficiently with a yield of 40–50%. The uptake of [18F]FPBZA by B16F0 melanoma cells was significantly higher than those by A375 tumor cells and NB-DNJ-pretreated B16F0 melanoma cells. B16F0 melanoma displayed prominent uptake of [18F]FPBZA at 2 h (7.81±0.82 %ID/g), compared with A375 tumor and inflammation lesion (3.00±0.71and1.67±0.56 %ID/g, resp.). [18F]FPBZA microPET scan clearly delineated B16F0 melanoma but not A375 tumor and inflammation lesion. In mice bearing pulmonary metastases, the lung radioactivity reached4.77±0.36 %ID/g at 2 h (versus1.16±0.23 %ID/g in normal mice).Conclusions. Our results suggested that [18F]FPBZA PET would provide a promising and specific approach for the detection of primary and metastatic melanoma lesions.
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Liu, Jia-Fang, Kuang Lai, Shu-Fen Peng, Pornsuda Maraming, Yi-Ping Huang, An-Cheng Huang, Fu-Shin Chueh, Wen-Wen Huang та Jing-Gung Chung. "Berberine Inhibits Human Melanoma A375.S2 Cell Migration and Invasion via Affecting the FAK, uPA, and NF-κB Signaling Pathways and Inhibits PLX4032 Resistant A375.S2 Cell Migration In Vitro". Molecules 23, № 8 (13 серпня 2018): 2019. http://dx.doi.org/10.3390/molecules23082019.
Повний текст джерелаАнотація:
Many studies have demonstrated that berberine inhibited the cell migration and invasion in human cancer cell lines. However, the exact molecular mechanism of berberine inhibiting the cell migration and invasion of human melanoma A375.S2 and A375.S2/PLX (PLX4032 induced resistant A375.S2) skin cancer cells remains unknown. In this study, we investigated the anti-metastasis mechanisms of berberine in human melanoma cancer A375.S2 cells and A375.S2/PLX resistant cells in vitro. Berberine at low concentrations (0, 1, 1.5 and 2 μM) induced cell morphological changes and reduced the viable cell number and inhibited the mobility, migration, and invasion of A375.S2 cells that were assayed by wound healing and transwell filter. The gelatin zymography assay showed that berberine slightly inhibited MMP-9 activity in A375.S2 cells. Results from western blotting indicated that berberine inhibited the expression of MMP-1, MMP-13, E-cadherin, N-cadherin, RhoA, ROCK1, SOS-1, GRB2, Ras, p-ERK1/2, p-c-Jun, p-FAK, p-AKT, NF-κB, and uPA after 24 h of treatment, but increased the PKC and PI3K in A375.S2 cells. PLX4032 is an inhibitor of the BRAFV600E mutation and used for the treatment of cancer cells harboring activated BRAF mutations. Berberine decrease cell number and inhibited the cell mobility in the resistant A375.S2 (A375.S2/PLX, PLX4032 generated resistant A375.S2 cells). Based on these observations, we suggest that the potential of berberine as an anti-metastatic agent in melanoma that deserves to be investigated in more detail, including in vivo studies in future.
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Huang, Dao Chao, Xian Fang Yang, Benoît Ochietti, Ibtihal Fadhil, Anne Camirand, and Richard Kremer. "Parathyroid Hormone-Related Protein: Potential Therapeutic Target for Melanoma Invasion and Metastasis." Endocrinology 155, no. 10 (October 1, 2014): 3739–49. http://dx.doi.org/10.1210/en.2013-1803.
Повний текст джерелаАнотація:
Abstract The role of PTHrP in the highly metastatic human melanoma disease is not known. This study investigates the mechanisms of action of this secreted factor through homozygous inactivation of the Pthrp gene in A375 human melanoma cells. In vitro, Pthrp-ablated cells (knockout [KO]-A375, −/−) showed decreased motility and anchorage-independent growth, rounder morphology, and a significant reduction in invasion capacity compared with nonablated A375 cells (wild-type [WT]-A375, +/+). PTHrP peptide 1–34 and conditioned medium from WT-A375 cells partially restored the invasive phenotype in KO-A375. Pthrp ablation substantially decreased actin polymerization, matrix metallopeptidase 9 expression and focal adhesion kinase phosphorylation. In vivo, green fluorescent protein-transduced ablated and nonablated A375 cells were injected intracardially or sc into nude mice to study proliferation and multiorgan metastasis. Dissemination of injected Pthrp-ablated cells to lung and liver was reduced by 85% and 50%, respectively, compared with nonablated controls (120 hours after injection). The number of metastatic lesions and the percentage of animals with metastasis were markedly lower in mice injected with Pthrp-ablated A375, and 45% of these animals survived a 7-week period compared with 15% of mice injected with nonablated WT-A375. When mice injected with WT-A375 were treated with our blocking anti-PTHrP monoclonal antibody raised against the first 33 amino acids of human PTHrP, tumor size was decreased by more than 80% over 4 weeks and survival was significantly improved over 8 months. This study provides direct evidence of the major role for PTHrP in melanoma invasion and metastasis and suggests that agents that suppress PTHrP may be beneficial against melanoma progression.
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Lachman, L. B., C. A. Dinarello, N. D. Llansa, and I. J. Fidler. "Natural and recombinant human interleukin 1-beta is cytotoxic for human melanoma cells." Journal of Immunology 136, no. 8 (April 15, 1986): 3098–102. http://dx.doi.org/10.4049/jimmunol.136.8.3098.
Повний текст джерелаАнотація:
Abstract Human peripheral blood monocytes stimulated with LPS were found to release an activity that was cytotoxic for the A375 melanoma. Biochemical and immunological characterization of the activity indicated that IL 1-beta was the cytotoxic agent. Human recombinant IL 1-beta, purified to homogeneity, was directly cytotoxic for A375. Tumor necrosis factor, also released by activated monocytes, was not cytotoxic for the A375 melanoma.
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Ge, Lan, Yaguang Wu, Ming Wan, Yi You, Zhifang Zhai, and Zhiqiang Song. "Metformin Increases Sensitivity of Melanoma Cells to Cisplatin by Blocking Exosomal-Mediated miR-34a Secretion." Journal of Oncology 2021 (November 29, 2021): 1–7. http://dx.doi.org/10.1155/2021/5525231.
Повний текст джерелаАнотація:
Melanoma, also known as malignant melanoma, is a type of cancer derived from the pigment-containing cells known as melanocytes. Cisplatin (CDDP) is widely used in the treatment of different types of tumors with high response rates, but it generally has low efficiency in melanoma. This study aimed to investigate whether metformin could sensitize the melanoma cell line A375 to cisplatin. Our results for the first time indicated that CDDP increased the miR-34a secretion by exosomes in melanoma A375 cells, which was, at least partially, related to the cisplatin resistance of melanoma cells. Moreover, metformin significantly sensitized A375 cells to cisplatin. Mechanistically, metformin significantly blocked the exosome-mediated miR-34a secretion induced by cisplatin. Our study not only reveals a novel mechanism that exosomal secretion of miR-34a is involved in the cisplatin resistance of melanoma cells but also provides a promising therapeutic strategy by synergistic addition of metformin.
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Freeman, Taylor, Samar Sayedyahossein, Danielle Johnston, Rafael Sanchez-Pupo, Brooke O’Donnell, Kenneth Huang, Zameena Lakhani, et al. "Inhibition of Pannexin 1 Reduces the Tumorigenic Properties of Human Melanoma Cells." Cancers 11, no. 1 (January 16, 2019): 102. http://dx.doi.org/10.3390/cancers11010102.
Повний текст джерелаАнотація:
Pannexin 1 (PANX1) is a channel-forming glycoprotein expressed in many tissues including the skin. PANX1 channels allow the passage of ions and molecules up to 1 kDa, including ATP and other metabolites. In this study, we show that PANX1 is highly expressed in human melanoma tumors at all stages of disease progression, as well as in patient-derived cells and established melanoma cell lines. Reducing PANX1 protein levels using shRNA or inhibiting channel function with the channel blockers, carbenoxolone (CBX) and probenecid (PBN), significantly decreased cell growth and migration, and increased melanin production in A375-P and A375-MA2 cell lines. Further, treatment of A375-MA2 tumors in chicken embryo xenografts with CBX or PBN significantly reduced melanoma tumor weight and invasiveness. Blocking PANX1 channels with PBN reduced ATP release in A375-P cells, suggesting a potential role for PANX1 in purinergic signaling of melanoma cells. In addition, cell-surface biotinylation assays indicate that there is an intracellular pool of PANX1 in melanoma cells. PANX1 likely modulates signaling through the Wnt/β-catenin pathway, because β-catenin levels were significantly decreased upon PANX1 silencing. Collectively, our findings identify a role for PANX1 in controlling growth and tumorigenic properties of melanoma cells contributing to signaling pathways that modulate melanoma progression.
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Liu, Wenjing, Xiaona Liu, Zhaohai Pan, Dan Wang, Minjing Li, Xiaoyu Chen, Ling Zhou, Maolei Xu, Defang Li, and Qiusheng Zheng. "Ailanthone Induces Cell Cycle Arrest and Apoptosis in Melanoma B16 and A375 Cells." Biomolecules 9, no. 7 (July 11, 2019): 275. http://dx.doi.org/10.3390/biom9070275.
Повний текст джерелаАнотація:
Malignant melanoma is the most lethal type of skin cancer. Previous studies have shown that ailanthone has potent antitumor activity in a variety of cell lines. However, the anti-tumor effect of ailanthone on malignant melanoma remains unclear. To investigate the anti-tumor mechanisms of ailanthone in human melanoma B16 and mouse melanoma A375 cells, the cell counting kit-8 assay, colony formation assay, DNA content analysis, Hoechst 33258, and Annexin V-FITC/PI staining were used to assess cell proliferation, cell cycle distribution, and cell apoptosis, respectively. Western blotting was performed to evaluate the expression of cell cycle- and apoptosis-related proteins and regulatory molecules. The results showed that ailanthone significantly inhibited melanoma B16 and A375 cell proliferation as well as remarkably induced cell cycle arrest at the G0–G1 phase in B16 cells and the G2–M phase in A375 cells in a dose-dependent manner. Further investigation revealed that ailanthone promoted the expression of p21 and suppressed the expression of cyclin E in B16 cells or cyclin B in A375 cells through the PI3K-Akt signaling pathway. In addition, ailanthone induced B16 and A375 cell apoptosis via a caspase-dependent mechanism. Further studies showed that ailanthone remarkably downregulated Bcl-2 and upregulated Apaf-1 and Bax, and subsequently increased mitochondrial membrane permeabilization and released cytochrome c from the mitochondria in B16 cells and A375 cells. Taken together, ailanthone induces cell cycle arrest via the PI3K-Akt signaling pathway as well as cell apoptosis via the mitochondria-mediated apoptotic signaling pathway. Ailanthone may be potentially utilized as an anti-tumor agent in the management of malignant melanoma.
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Park, Jaehyun, Mijin Kwon, Jaehoon Lee, Sangkyu Park, Jeongmin Seo, and Sangho Roh. "Anti-Cancer Effects of Lactobacillus plantarum L-14 Cell-Free Extract on Human Malignant Melanoma A375 Cells." Molecules 25, no. 17 (August 26, 2020): 3895. http://dx.doi.org/10.3390/molecules25173895.
Повний текст джерелаАнотація:
Human malignant melanoma is the most aggressive type of skin cancer with high metastatic ability. Despite several traditional therapies, the mortality rate remains high. Lactobacillus plantarum (L. plantarum), a species of lactic acid bacteria (LAB), is being studied for human health, including cancer treatment. However, few studies have elucidated the relationship between L. plantarum extract and human malignant melanoma. To investigate the effects of L. plantarum on human melanoma cells, A375 human melanoma cells were used and treated with L. plantarum L-14 extract. After the treatment, viability, migration ability, molecular changes of migration- and apoptosis-related genes, and the location of cytochrome c was evaluated. The L-14 extract inhibited the viability, migration of A375 cells as well as reduced expression of migration-related genes. In addition, it was confirmed that the L-14 extract induced intrinsic apoptosis in A375 cells. This study demonstrated that the L-14 extract exerted anticancer effects on A375 cells. Therefore, these data suggest that the L-14 extract is worth studying for the development of melanoma drugs using LAB.
Дисертації з теми "A375 Melanoma cells"
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Herwig, Nadine. "Der RAGE-Ligand S100A4." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-214035.
Повний текст джерелаАнотація:
Das maligne Melanom zählt zu den aggressivsten und behandlungsresistentesten aller Krebsarten. In den letzten 20 Jahren hat sich die Rate der Melanom-Erkrankungen innerhalb der weißen Bevölkerung verdreifacht.
Mittlerweile liegen eine Reihe von Untersuchungen zu den molekularbiologischen Mechanismen der Entwicklung und Progression des malignen Melanoms vor. Aktuelle Forschungsvorhaben beschäftigen sich vor allem mit der Identifizierung Melanom-spezifischer Biomarker, die diagnostische und prognostische Informationen liefern sowie die Entwicklung einer zielgerichteten, kombinierten und individualisierten Therapie des metastasierenden Melanoms ermöglichen. In diesem Kontext soll die vorliegende Arbeit einen weiteren Beitrag zum Verständnis der Metastasierungskaskade und der daran beteiligten Proteine leisten.
Aufgrund der Überexpression in einer Reihe von Tumoren und seiner geringen Molmasse von lediglich 11,5 kDa bietet sich das S100A4-Protein als Marker mit hoher prognostischer Signifikanz für verschiedene Tumorentitäten an. Jedoch ist die Beteiligung von S100A4 bei der Ausbildung des invasiven Tumorphänotyps noch nicht vollständig aufgeklärt. S100A4 besitzt zahlreiche intra- und extrazelluläre Bindungspartner, wobei die Metastasierung scheinbar ausschließlich durch das extrazelluläre Protein beeinflusst wird. S100A4 wechselwirkt extrazellulär beispielsweise mit dem Rezeptor für fortgeschrittene Glykierungsendprodukte (RAGE). Ziel dieser Arbeit war es, speziell die Bedeutung von S100A4 und seiner Interaktion mit RAGE für das prometastatische Verhalten von Melanomzellen in vitro und in vivo näher zu charakterisieren. Darüber hinaus sollte die Beteiligung von S100A4 bei der Gehirn-Metastasierung untersucht werden, wobei insbesondere die Regulierung der Endothelzell-Permeabilität und der transendothelialen Migration der Melanomzellen im Vordergrund stand.
Im Rahmen dieser Arbeit wurde gezeigt, dass S100A4 und die Interaktion mit RAGE die prometastatischen Eigenschaften der A375-Melanomzellen förderte. Zudem verringerte extrazelluläres S100A4 die Zell-Integrität von Gehirn-Endothelzellen und erleichterte somit die Durchdringung der Blut-Hirn-Schranke. Diese Erkenntnis lässt sich möglicherweise auf andere Blut-Gewebe-Schranken übertragen. Die In-vivo-Orientierungsstudie zeigte, dass S100A4- und RAGE-überexprimierende Zellen zu einer verstärkten disseminierten Metastasierung führten, wobei sich zwei unterschiedliche Verteilungsmuster ergaben. Darüber hinaus führten beide Zelllinien vereinzelt zur Bildung von Gehirnmetastasen, wodurch sich die intrakardiale Injektion durchaus als Modell für weitere Therapiestudien mit dem Augenmerk der S100A4-RAGE-stimulierten Metastasierung eignet. Die genauere Kenntnis regulativer Mechanismen bei der Synthese und Sekretion von S100A4 sowie die pathophysiologische Differenzierung der S100A4-Interaktion mit RAGE eröffnen neue Wege, die S100A4-vermittelten Effekte therapeutisch zu beeinflussen. Daraus lassen sich möglicherweise neue zielgerichtete Radionuklid-basierte Therapieansätze für das metastasierende Melanom ableiten.
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Kováč, Ján. "Porovnání různých metod aminace polykaprolaktonu z hlediska jejich efektivnosti pro tkáňové inženýrství." Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2020. http://www.nusl.cz/ntk/nusl-433015.
Повний текст джерелаАнотація:
This diploma thesis dealt with the comparison of different methods of amination of polycaprolcatone in terms of their effectiveness for tissue engineering. A polycaprolactone membrane was prepared by an electrospinning method, which was subsequently modified by three different amination methods. Selected types of amination were plasma polymerization with cyclopropylamine monomer, hybrid modification using plasma and N-allylmethylamine monomer, and chemical amination using aminolysis with diaminohexane. Surface amines were subsequently characterized by electron scanning microscopy (SEM), X-ray photoelectron spectroscopy (XPS), attenuated total reflection infrared spectroscopy (ATR-FTIR) and contact angle measurement. A cell culture designated A375 (Human malignant melanoma cell lines A375® CRL-1619®) was cultured on the thus modified membranes, which was analyzed by optical microscopy, and a proliferation assay was performed by determining the relative amount of ATP. Based on the experimental results, we can confirm the success for all types of amination. In terms of efficiency for tissue engineering, the amination method by plasma polymerization with the monomer cyclopropylamine has the most satisfactory results.
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Greeff, Christopher Whitney 1961. "CYTOGENETIC ABNORMALITIES AND THE PROGRESSION TO INVASION IN A375P HUMAN MELANOMA CELLS IN VITRO." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276462.
Повний текст джерелаАнотація:
A study was undertaken to determine whether cytogenetic abnormalities can be identified in an invasive melanoma cell population that has been selected in vitro out of a larger cell population of low invasive potential. The selecting agent was a denuded human amniotic membrane situated within Mega-Membrane Invasion Culture System chambers. Invasive cells were collected, grown, and harvested for cytogenetic analysis. Metaphases of these cells were examined for chromosomal abnormalities and for evidence of gene amplification in the form of double minute chromosomes. Invasive cell lines evinced changes in their degree of aneuploidy which were not seen in parental control lines of the same passage number. Significant karyotypic abnormalities identified in invasive cell lines were an increased dosage of chromosome 7 and multiple 1q translocation marker chromosomes. Double minute chromosomes were found in up to 18% of invasive cell metaphases examined and in 3% of parental controls. The incidence of double minutes was found to decrease as a function of passage number.
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Sung, Shu-Chiao, and 宋淑嬌. "The molecular mechanismof plumbagin in human melanoma A375.S2 cells." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/87434075810793523615.
Повний текст джерелаАнотація:
碩士嘉南藥理科技大學
化妝品科技研究所
95
This study is the first to investigate the anticancer effect of plumbagin in human melanoma A375.S2 cells. Plumabagin exhibited effective cell growth inhibition by inducing cancer cells to undergo S-G2/M phase arrest and apoptosis. Further investigation revealed that plumbagin’s inhibition of cell growth was also evident in a nude mice model. Blockade of cell cycle was associated with increased levels of p21, and reduced amounts of cyclinB1, cyclinA, cdc2 and cdc25C. Plumbagin also enhanced the levels of inactivated phosphorylated cdc2 and cdc25C. Plumbagin triggered the mitochondrial apoptotic pathway indicated by a change in Bax/Bcl-2 ratios, resulting in caspase-9 activation. We also found the generation of ROS is a critical mediator in plumbagin-induced cell growth inhibition. Antioxidants vitamin C and catalase significantly decreased apoptosis. In addition, plumbagin also increased the activation of ASK and then enhanced the phosphorylation of JNK and ERK1/2, but not p38. Moreover, blocking ERK and JNK by specific inhibitors suppressed plumbagin-induced apoptosis. Taken together, these results imply a critical role for ROS and JNK in the plumbagin’s anticancer activity.
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"Growth inhibitory effect of docosahexaenoic acid on human melanoma A375 cells." 2007. http://library.cuhk.edu.hk/record=b5896766.
Повний текст джерелаАнотація:
Tong, Kit Fong.Thesis (M.Phil.)--Chinese University of Hong Kong, 2007.
Includes bibliographical references (leaves 91-104).
Abstracts in English and Chinese.
Abstract --- p.i
Acknowledgements --- p.vi
Table of Contents --- p.vii
List of Figures --- p.x
List of Tables --- p.xii
List of Abbreviations --- p.xiii
Chapter Chapter 1 --- Introduction --- p.1
Chapter 1.1 --- Cancer --- p.2
Chapter 1.1.1 --- Tumor development --- p.2
Chapter 1.1.2 --- Cell cycle --- p.4
Chapter 1.1.3 --- Apoptosis --- p.9
Chapter 1.1.3.1 --- The extrinsic pathway --- p.14
Chapter 1.1.3.2 --- The intrinsic pathway --- p.16
Chapter 1.1.3.3 --- The Bcl-2 family proteins --- p.17
Chapter 1.1.3.4 --- Execution of apoptosis --- p.20
Chapter 1.1.4 --- Melanoma --- p.22
Chapter 1.2 --- Polyunsaturated fatty acids (PUFAs) --- p.24
Chapter 1.2.1 --- "Chemistry, classification, metabolic conversion and sources …" --- p.24
Chapter 1.2.2 --- Epidemiology studies --- p.27
Chapter 1.2.3 --- Docosahexaenoic acid (DHA) --- p.28
Chapter 1.2.3.1 --- Sources --- p.28
Chapter 1.2.3.2 --- DHA and cancer --- p.29
Chapter 1.3 --- Objectives --- p.33
Chapter Chapter 2 --- Materials and Methods --- p.34
Chapter 2.1 --- In vitro studies of DHA on growth and survival of human cancer cells --- p.34
Chapter 2.1.1 --- Cell cultures --- p.34
Chapter 2.1.2 --- Studies of growth inhibition of DHA on human cancer cells --- p.35
Chapter 2.1.2.1 --- MTT assay --- p.35
Chapter 2.1.2.2 --- Chemiluminescent-bromodeoxyuridine (Chemi-BrdU) immunoassay --- p.36
Chapter 2.1.3 --- Studies of growth inhibitory mechanism of DHA on A375 cells. --- p.38
Chapter 2.1.3.1 --- DNA -flow cytometry analysis --- p.38
Chapter 2.1.3.2 --- Western blot analysis --- p.39
Chapter 2.1.3.3 --- Caspase inhibitor studies --- p.42
Chapter 2.1.3.4 --- Mitochondrial membrane potential analysis --- p.42
Chapter 2.2 --- In vivo study of the anticancer effect of DHA on A375 cells --- p.44
Chapter 2.2.1 --- Animals --- p.44
Chapter 2.2.2 --- Cell inoculation and treatments --- p.44
Chapter 2.2.3 --- Western blot analysis --- p.45
Chapter 2.3 --- Statistical analysis --- p.46
Chapter Chapter 3 --- Results --- p.47
Chapter 3.1 --- In vitro studies of DHA on growth and survival of human canccr cells --- p.47
Chapter 3.1.1 --- DHA reduced proliferation and survival of human cancer cells --- p.47
Chapter 3.1.2 --- DHA modulated cell cycle of A375 cells --- p.52
Chapter 3.1.3 --- DHA induced apoptosis in A375 cells --- p.55
Chapter 3.1.4 --- Caspase activations were involved in the DHA-induced apoptosis in A375 cells --- p.59
Chapter 3.1.5 --- "Caspase 3´ة 6, 8 and 9 were activated in DHA-induced apoptosis of A375 cells" --- p.62
Chapter 3.1.6 --- DHA dissipated mitochondrial membrane potential in A375 cells --- p.66
Chapter 3.1.7 --- DHA triggered the mitochondrial pathway of apoptosis --- p.68
Chapter 3.1.8 --- DHA triggered the death receptor pathway of apoptosis --- p.71
Chapter 3.2 --- In vivo study of the anticancer effect of DHA on A375 cells --- p.74
Chapter 3.2.1 --- Effect of DHA on the growth ofA375 xenograft in athymic Bαlb/c mice --- p.74
Chapter 3.2.2 --- DR4 and TRAIL were upregulated by DHA treatment in A375 solid tumor --- p.77
Chapter Chapter 4 --- Discussion --- p.79
References --- p.91
6
Wu, Liu-Wei, and 吳律緯. "Benzyl Isothiocyanate Induces Growth Inhibition and Cell Apoptosis in Human Melanoma A375.S2 Cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/06797224513531439776.
Повний текст джерелаАнотація:
碩士亞洲大學
生物科技學系碩士班
98
Skin cancer is one of the common carcinomatous diseases. It is becoming increasingly common in younger populations.Recently, many reports indicated that increased intake of cruciferous vegetables may be effective in preventing the risk of cancer and to reduce the incidence of cancer. Benzyl isothiocyanate (BITC), a compound presented in cruciferous vegetables, had shown to induce cell cycle arrest and apoptosis in many cancer cells. There is no report to show BITC inhibited the growth of A375.S2 human skin cancer cells. In this study BITC affecting apoptosis in A375.S2 cells was investigated. MTT assay was used to measure cell viability of A375.S2 cells after BITC treatment. DNA damage was determined by DNA fragmentation assay, DAPI staining and Comet assay. Flow cytometric analysis was performed to investigate the levels of mitochondrial membrane potential (ΔΨm), the production of reactive oxygen species (ROS), intracellular Ca2+ release and cell cycle distribution. Finally, we used the flow cytometry to examine caspase-3 activity and Annexin V affinity assay for apoptosis. In western blotting assay, we found cytochrome c, AIF and Endo G were released from mitochondria and activated downstream pathway to cause cell apoptosis. Our results showed that BITC treatment for 24 h significantly reduced the cell survival with an IC50 of 10±0.5 μM. BITC induced cell cycle arrest at G2/ M phase in A375.S2 cells. Moreover, BITC also caused DNA damage, decreased ΔΨm and increased ROS and intracellular Ca2+ levels. These observations indicate that BITC could induce apoptosis in human melanoma A375.S2 cell.
7
Chang, Ya-hui, and 張雅惠. "Involvement of ROS in Vanadate Potentiated H2O2 Induced Apoptosis in Human Melanoma A375 Cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/09262952349394332375.
Повний текст джерелаАнотація:
碩士輔英科技大學
生物技術系碩士班
98
Vanadate is an environmentally toxic metal with peculiar and sometimes contradictory cellular effects. Studies concerning the mechanisms of action of vanadate showed to induce gene expressions, oxidative burst, changes in cytosolic calcium, tyrosine phosphorylation, insulin-mimetic effects and also cytoskeletal alterations, but the regulation mechanisms remain to be elucidated. Hydrogen peroxide（H2O2）is a strong oxide which can induce stress in culture cells and play a role in the physiological mode in the processes of growth, differentiation and the death control. We found that human melanoma A375 cells were relatively more sensitive than human lung carcinoma NCI-H460 cells to the cytotoxic effects induced by H2O2 as well as sodium vanadate. In this study, the role of intracellular oxidative stress in the mechanism of action was studied using the H2O2, vanadate, and H2O2 plus vanadate in the three cells. The proliferation and viability as well as protein expressions of sub-toxic dosage H2O2 treated cells were detected in the prensence of different concentrations of vanadate for different durations. Our data demonstrated up to 1.25μM of vanadate had no effect on proliferation and viability of A375 cells, but cotreated cells with vanadate and H2O2 resulted in rapidly cell growth inhibition and apoptotic cells became more abundant. Vanadate seems to have synergistic effects to enhance cytotoxicity of H2O2 in A375 cells depending on the dose-and time. The fragmentation of DNA, cell cycle distribution and generation of ROS as well as of were observed by using of flow cytometry in H2O2 and vanadate treated cells for providing other cytotoxic mechanisms. However, the antioxidant N-acetyl cysteine, a reactive oxygen species inhibitor, greatly diminished the intracellular oxidation and protein phosphotyrosine accumulation as well as the H2O2 induced cytotoxicity which potentiated by vanadate. These results indicate a role for oxidative stress in the biological effects of PTP inhibitor vanadate in H2O2 treated cells.
8
"Baicalein induces caspase-dependent apoptosis in human melanoma A375 cells associated with elicitation of intrinsic and extrinsic apoptotic pathways." 2007. http://library.cuhk.edu.hk/record=b5896768.
Повний текст джерелаАнотація:
Li, Wing Yan Kate.Thesis (M.Phil.)--Chinese University of Hong Kong, 2007.
Includes bibliographical references (leaves 130-154).
Abstracts in English and Chinese.
Acknowledgements --- p.i
Abstract --- p.iii
Abstract (Chinese Version) --- p.vi
Table of Contents --- p.viii
List of Figures --- p.xiii
List of Abbreviations --- p.xv
Chapter Chapter 1 --- General Introduction
Chapter 1.1. --- Overview of cancer --- p.1
Chapter 1.2. --- Apoptosis and cancer --- p.4
Chapter 1.3. --- Roles and regulation of caspase-dependent apoptosis --- p.7
Chapter 1.3.1. --- Extrinsic death receptor pathway --- p.8
Chapter i. --- TNFR1 and TNFa --- p.13
Chapter ii. --- CD95/Fas and CD95 Ligand/FasL --- p.14
Chapter iii. --- "TRAIL-R1(DR4), TRAIL-R2 (DR5) and TRAIL" --- p.14
Chapter 1.3.2. --- Intrinsic mitochondrial pathway --- p.16
Chapter i. --- Bcl-2 family of proteins --- p.17
Chapter ii. --- Reactive Oxygen Species (ROS) --- p.19
Chapter 1.4. --- Phytochemicals from Traditional Chinese Medicine (TCM) as a source of new therapeutics --- p.22
Chapter 1.5. --- Biological effects of baicalein --- p.25
Chapter 1.5.1 --- Roles of baicalein as a lipoxygenase inhibitor --- p.28
Chapter 1.5.2 --- Dual roles of baicalein as an antioxidant and prooxidant --- p.28
Chapter 1.5.3 --- "Roles of baicalein as an anti-carcinogenic, anti-proliferative and anti-metastatic agent" --- p.29
Chapter 1.6. --- Aims of current study --- p.30
Chapter Chapter 2 --- Effects of Baicalein on Growth and Survival of Human Cancer Cells
Chapter 2.1 --- Introduction --- p.33
Chapter 2.2 --- Materials and Methods
Chapter 2.2.1 --- Cell culture --- p.35
Chapter 2.2.2 --- Measurement of growth and survival of various cell lines --- p.36
Chapter 2.2.3 --- Statistical analysis --- p.37
Chapter 2.3 --- Results
Chapter 2.3.1 --- Baicalein retards the growth and survival of human melanoma A375 and colorectal carcinoma Caco-2 --- p.37
Chapter 2.3.2 --- Baicalein reduces the growth and survival of melanoma A375 but not in normal skin fibroblast Hs68 cells --- p.40
Chapter 2.4 --- Discussion --- p.42
Chapter Chapter 3 --- Effects of Baicalein on Cell Cycle and the Apoptosis in Human Melanoma A375 Cells
Chapter 3.1 --- Introduction --- p.44
Chapter 3.2 --- Materials and Methods
Chapter 3.2.1 --- Determination of cell cycle changes and quantification of apoptosis --- p.51
Chapter 3.2.2 --- Immunoblotting --- p.52
Chapter 3.2.3 --- Inhibition of caspase-8 by caspase-8 inhibitor --- p.54
Chapter 3.2.4 --- Fluorometric measurement of caspase-3 activity --- p.54
Chapter 3.2.5 --- Statistical analysis --- p.55
Chapter 3.3 --- Results
Chapter 3.3.1 --- Baicalein induces S-phase arrest in cell cycle and triggers apoptosis --- p.55
Chapter 3.3.2 --- Baicalein induces proteolytic inactivation of PARP and activation of caspases --- p.59
Chapter 3.3.3 --- Caspase-8 is the major initiator caspase eliciting the baicalein-induced apoptosis --- p.62
Chapter 3.4 --- Discussion --- p.67
Chapter Chapter 4 --- Effects of Baicalein on the Extrinsic Apoptotic Pathways in Human Melanoma A375 Cells
Chapter 4.1 --- Introduction --- p.72
Chapter 4.2 --- Materials and Methods
Chapter 4.2.1 --- Immunoblotting --- p.75
Chapter 4.2.2 --- Determination of sub-lethal dose of exogenous TRAIL --- p.76
Chapter 4.2.3 --- Determination of the combinatory effect of exogenous TRAIL and baicalein --- p.76
Chapter 4.2.4 --- Statistical analysis --- p.77
Chapter 4.3 --- Results
Chapter 4.3.1 --- Baicalein upregulates the expressions of death receptor 4 (DR4) and death receptor 5 (DR5) --- p.77
Chapter 4.3.2 --- Baicalein sensitizes the melanoma cells to sub-lethal dose of exogenous TRAIL --- p.80
Chapter 4.4 --- Discussion --- p.84
Chapter Chapter 5 --- Effects of Baicalein on the Extrinsic Apoptotic Pathways in Human Melanoma A375 Cells Cancer Cells
Chapter 5.1 --- Introduction --- p.88
Chapter 5.2 --- Materials and Methods
Chapter 5.2.1 --- Analysis of mitochondrial membrane potential --- p.94
Chapter 5.2.2 --- Fractionation of cell lysates into cytosolic and mitochondrial fractions for immunoblotting --- p.95
Chapter 5.2.3 --- Immunoblotting --- p.95
Chapter 5.2.4 --- Determination of cellular reactive oxygen species (ROS) production --- p.96
Chapter 5.2.5 --- Verification of ROS generation via the addition of Trolox´ёØ --- p.96
Chapter 5.2.6 --- Statistical analysis --- p.97
Chapter 5.3 --- Results
Chapter 5.3.1 --- Baicalein induces mitochondrial membrane depolarization --- p.97
Chapter 5.3.2 --- Cytochrome c is released in the baicalein-induced mitochondrial membrane depolarization --- p.100
Chapter 5.3.3 --- Baicalein does not elicit the intrinsic apoptotic pathway via modulation of some better-characterized Bcl-2 family proteins in A375 cells --- p.102
Chapter 5.3.4 --- Baicalein induces ROS production --- p.105
Chapter 5.3.5 --- Baicalein induces mitochondrial permeabilization via ROS-mediated mechanisms --- p.108
Chapter 5.4 --- Discussion --- p.112
Chapter Chapter 6 --- General Discussion --- p.119
References --- p.130
9
raineri, alice. "Influence of ONCONASE in the therapeutic potential of PARP and BRAF inhibitors in human A375 melanoma cells." Doctoral thesis, 2019. http://hdl.handle.net/11562/1016949.
Повний текст джерелаАнотація:
Melanoma is one of the most aggressive form of skin cancer, characterized by high mortality rate due to the metastatic potential of its cells. Several therapies have been approved during last few years. Recently, the melanoma molecular characterization led to development of drugs acting against specific targets. For instance, BRAF inhibitors (BRAFi) have been tested against BRAF-mutated melanoma. Unfortunately, all chemotherapy strategies failed for the resistance acquired by tumor cells. Poly (ADP-ribose) polymerase (PARP) enzymes are crucial in the DNA damage response and the PARP inhibition causes the accumulation of unrepaired DNA, inducing cell death. PARP inhibitors (PARPi) are commonly used in chemotherapy. The most used PARPi in cancer therapy is olaparib, although it can be quickly throwing outside the cells by the P-glycoprotein drug efflux transporter. For this reason, a new PARPi generation has been designed, such as AZD2461 that demonstrated a lower binding affinity to the P-glycoprotein than olaparib. In vitro and in vivo studies showed that the protein onconase (ONC) exerted an antitumor effect in different cancer types, due to its ribonuclease activity. Therefore, in this work, the ONC effects on A375 human melanoma cell line that harbors a mutation in the BRAF kinase gene, has been evaluated. A reduction in A375 cell viability has been observed with ONC treatment, while no cytotoxicity was registered in normal human melanocytes. In A375 cells a reduction in BrdU incorporation and a decrease in Ki67 protein expression occurred, suggesting that ONC elicits a cytostatic effect. In addition, an increase of both Annexin V-FITC fluorescence and cleaved PARP1 expression level were observed, suggesting that ONC induces apoptotic cell death. In order to investigate the ONC intracellular targets, changes in the proteome profile have been investigated using mass spectrometry. A decreased expression level of proteins involved in telomere elongation, in the mesenchymal cell development and in the ribosomal subunit biogenesis has been obtained. A decrease in protein synthesis in ONC-treated cells was also demonstrated. Besides ONC, AZD2461 PARPi can reduce A375 cell viability, conversely, no strong benefits were obtained when ONC was administered in combination with AZD2461, in comparison with each single drug treatment. ONC and AZD2461 have displayed an inhibitory effect on both TNF-α gene transcription and NF-κB DNA binding activity, but no additive effect was observed when they were used in combination. In order to obtain A375 cells resistant to AZD2461, cells were treated for two months with AZD2461, but this long treatment did not induce resistance. Nevertheless, the AZD2461 long-time treated cells resulted more responsive to the ONC pro-apoptotic action, if compared to the parental ones. Subsequently, resistance against the BRAFi dabrafenib has been induced in A375 since long time treatment with increasing drug concentrations of dabrafenib induced a sorting of an A375 resistant cell (A375DR) subpopulation. A375DR cells displayed activation of the cancer stem cells markers CD133 and NANOG and increase expression of epithelial-mesenchymal transition-related proteins N-cadherin and nuclear β-catenin, in comparison with A375 parental (A375P) cells. In addition, A375DR showed an increase in the ERK1/2 phosphorylation level, suggesting a reactivation of the MAPK pathway. By comparing A375P and A375DR, ONC treatment can inhibit the total viability and the proliferation rate in both cell subpopulations and induce apoptotic cell death. Moreover, among its pleiotropic effects, ONC reduced nuclear p65 NF-κB amount and IκB kinase phosphorylation level, as well as metalloproteinase-2 activity in both cell subpopulations. Finally, ONC decreased cell colony formation, migration and invasion capability more extensively in A375DR than in A375P cells. In conclusion, ONC successfully counteracts malignant phenotype of A375 cells especially in BRAFi resistant cells and could become a helpful tool for therapy of melanoma recurrence.
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Yuan, Shang-wen, and 袁上雯. "The Effect of Shikonin on N-acetylation of 2-aminofluorene and Cell Growth in Human Malignant Melanoma Cells (A375.S2)." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/42603953315199017087.
Повний текст джерелаАнотація:
碩士中國醫藥學院
中西醫結合研究所
91
Shikonin is one of the components of Lithospermum erythrorhizon (Chinese herb medicine) used for skin infection and allergy for many generations in the Chinese population. In this study, shikonin was used to determine the inhibition of N-acetylation of 2-aminofluorence (2-AF) in human malignant melanoma cell line (A357.S2). The amounts of N-acetylation and non-N-acetylation of 2-AF were measured by high performance liquid chromatography. The results demonstrated that N-acetylation of AF from examined systems were decreased by shikonin in a dose-dependent manner. We also found out that this effect of shikonin on N-aectylation of AF also was time-course dependent. Apparently shikonin affect N-acetylation of AF in human malignant melanoma cell line (A357.S2). We investigated how shikonin affects human malignant melanoma cells (A375.S2) for determining the inhibition of cell growth, morphological changes, DNA fragmentation, and cell cycle by using flow cytometric assay and DNA gel electrophoresis. After exposure of the cells to shikonin which resulted in cell cycle arrest and cell death through apoptosis. This effect is also dose-dependent manner. Exposure of A375.S2 cells to shikonin induced expression of the cyclins and cyclin-dependent kinases (CDK) activity. These studies demonstrated that cyclins and CDKs play a key role in the inhibition of shikonin-induced apoptosis and cell cycle arrest in A375.S2 cells. This is the first findings to show shikonin affect human malignant melanoma cell lines (A375.S2).
Частини книг з теми "A375 Melanoma cells"
1
Hsieh, Jung-Feng, Shui-Tein Chen, and Sun-Long Cheng. "Molecular Profiling of A375 Human Malignant Melanoma Cells Treated with Kojic Acid and Arbutin." In Breakthroughs in Melanoma Research. InTech, 2011. http://dx.doi.org/10.5772/20019.
Повний текст джерелаТези доповідей конференцій з теми "A375 Melanoma cells"
1
Apostol, A., J. Biggerstaff, A. Dogariu, and Kimberly Olvey. "Near-Field Fluorescence Imaging of A375 Human Melanoma Cells." In Biomedical Topical Meeting. Washington, D.C.: OSA, 2002. http://dx.doi.org/10.1364/bio.2002.mi5.
Повний текст джерела
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Kaoud, Tamer S., William H. Johnson, Nancy D. Ebelt, Andrea Piserchio, Mangalika Warthaka, Micael Cano, Rachel Sammons, et al. "Abstract 3771: Discovery of a covalent inhibitor of ERK docking-interactions that inhibits A375 melanoma cells proliferation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3771.
Повний текст джерела
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Syed, Deeba N., Rahul K. Lall, Mohammad Imran Khan, Maria Shabbir, and Hasan Mukhtar. "Abstract 3125: Fisetin inhibits p90RSK/YB-1 signaling and downregulates chemoresistance associated P-glycoprotein in A375 melanoma cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3125.
Повний текст джерела
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Jimenez, Benilde, and Jose L. Orgaz. "Abstract LB-310: Changes in the gene expression profile of A375 human melanoma cells induced by over-expression of multifunctional pigment epithelium-derived factor." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-310.
Повний текст джерела
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Maksimovic, Sinisa. "Abstract A37: The signet ring cell melanoma - rare morphological variant of melanoma: Case report." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-a37.
Повний текст джерела
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Wentworth, Lucy, David A. Mahvi, Justin V. Meyers, Samantha Durbin, and Clifford S. Cho. "Abstract A37: CTLA-4 blockade improves the balance of CD8+ effector and CD4+ regulatory T cells following adoptive cell transfer melanoma immunotherapy." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a37.
Повний текст джерела
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Aris, Mariana, María Betina Pampena, Estrella M. Levy, Alicia I. Bravo, Florencia P. Madorsky-Rowdo, Ana Mordoh, Julio Kaplan, et al. "Abstract A37: Immunization of cutaneous melanoma patients with the allogeneic cell vaccine CSF-470 enhances immune infiltration of metastatic lesions and would favor subsequent response to Vemurafenib." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a37.
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