https://scholars.lib.ntu.edu.tw/handle/123456789/544506
標題: | Characterization of molecular events in a series of bladder urothelial carcinoma cell lines with progressive resistance to arsenic trioxide | 作者: | Hour T.-C. CHAO-YUAN HUANG CHIA-CHI LIN Chen J. Guan J.-Y. Lee J.-M. YEONG-SHIAU PU |
公開日期: | 2004 | 卷: | 15 | 期: | 8 | 起(迄)頁: | 779-785 | 來源出版物: | Anti-Cancer Drugs | 摘要: | Our previous studies have shown that arsenic trioxide (As2O 3), a novel anti-cancer agent, may be active against urothelial carcinomas. A series of bladder urothelial carcinoma cells with progressive As2O3 resistance were established and studied to reveal molecular events in relation to the mechanisms of resistance to As 2O3. A sensitive parental line (NTUB1) and three As 2O3-resistant sublines (NTUB1/As) were used with their IC50s being 0.9, 1.2, 2.5 and 4.9 μM, respectively. Cellular resistance to As2O3 was associated with a lowered proliferation profile (increased p53 and p21Waf1/Cip1 and decreased c-Myc levels) and a greater resistance to apoptosis (elevated Bcl-2 levels). Cells with a stronger resistance had higher expressions of superoxide dismutase (Cu/Zn) and hMSH2 (but not hMLH1). GSH contents were up-regulated in resistant cells in a dose-dependent manner. The DNA-binding activities of NF-κB and AP-1 were down-regulated in resistant cells in a dose-dependent manner. Profound molecular alterations occur during the acquisition of secondary As 2O3 resistance. Our in vitro cellular model may help to reveal resistance mechanisms to As2O3 in bladder urothelial carcinoma cells. ? 2004 Lippincott Williams & Wilkins. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-4644320306&doi=10.1097%2f00001813-200409000-00007&partnerID=40&md5=a11957d4e126457acfb2aec7093890f6 https://scholars.lib.ntu.edu.tw/handle/123456789/544506 |
ISSN: | 0959-4973 | DOI: | 10.1097/00001813-200409000-00007 | SDG/關鍵字: | antineoplastic agent; arsenic trioxide; copper zinc superoxide dismutase; glutathione; immunoglobulin enhancer binding protein; Myc protein; protein bcl 2; protein MLH1; protein MSH2; protein p21; protein p53; reactive oxygen metabolite; transcription factor AP 1; apoptosis; article; bladder carcinoma; cancer resistance; carcinoma cell; cell proliferation; controlled study; DNA repair; dose response; gel mobility shift assay; human; human cell; IC 50; priority journal; protein DNA binding; protein expression; Western blotting; Apoptosis; Arsenicals; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cyclin-Dependent Kinase Inhibitor p21; DNA-Binding Proteins; Dose-Response Relationship, Drug; Down-Regulation; Drug Evaluation, Preclinical; Drug Resistance, Neoplasm; Electrophoretic Mobility Shift Assay; Forecasting; Glutathione; Humans; Inhibitory Concentration 50; MutS Homolog 2 Protein; NF-kappa B; Oxides; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; Reactive Oxygen Species; Superoxide Dismutase; Transcription Factor AP-1; Transcription Factors; Tumor Suppressor Protein p53; Up-Regulation; Urinary Bladder Neoplasms; Urothelium |
顯示於: | 醫學系 |
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