https://scholars.lib.ntu.edu.tw/handle/123456789/544440
標題: | Transcriptional up-regulation of SOD1 by CEBPD: A potential target for cisplatin resistant human urothelial carcinoma cells | 作者: | Hour T.-C. Lai Y.-L. Kuan C.-I. Chou C.-K. Wang J.-M. Tu H.-Y. Hu H.-T. Lin C.-S. Wu W.-J. YEONG-SHIAU PU Sterneck E. Huang A.-M. |
關鍵字: | C/EBP transcription factor; Cisplatin drug resistance; SOD inhibitor; Superoxide dismutase; Urothelial carcinoma | 公開日期: | 2010 | 卷: | 80 | 期: | 3 | 起(迄)頁: | 325-334 | 來源出版物: | Biochemical Pharmacology | 摘要: | Bladder cancer is the fourth most common type of cancer in men (ninth in women) in the United States. Cisplatin is an effective agent against the most common subtype, urothelial carcinoma. However, the development of chemotherapy resistance is a severe clinical problem for the successful treatment of this and other cancers. A better understanding of the cellular and molecular events in response to cisplatin treatment and the development of resistance are critical to improve the therapeutic options for patients. Here, we report that expression of the CCAAT/enhancer binding protein delta (CEBPD, C/EBPδ, NF-IL6β) is induced by cisplatin in the human bladder urothelial carcinoma NTUB1 cell line and is specifically elevated in a cisplatin resistant subline. Expression of CEBPD reduced cisplatin-induced reactive oxygen species (ROS) and apoptosis in NTUB1 cells by inducing the expression of Cu/Zn-superoxide dismutase (SOD1) via direct promoter transactivation. Several reports have implicated CEBPD as a tumor suppressor gene. This study reveals a novel role for CEBPD in conferring drug resistance, suggesting that it can also be pro-oncogenic. Furthermore, our data suggest that SOD inhibitors, which are already used as anti-angiogenic agents, may be suitable for combinatorial chemotherapy to prevent or treat cisplatin resistance in bladder and possibly other cancers. ? 2010 Elsevier Inc. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-77953359913&doi=10.1016%2fj.bcp.2010.04.007&partnerID=40&md5=df2bb051cfa7cca64ab51e8650c6d022 https://scholars.lib.ntu.edu.tw/handle/123456789/544440 |
ISSN: | 0006-2952 | DOI: | 10.1016/j.bcp.2010.04.007 | SDG/關鍵字: | arsenic trioxide; CCAAT enhancer binding protein delta; cisplatin; copper zinc superoxide dismutase; gemcitabine; paclitaxel; reactive oxygen metabolite; apoptosis; article; bladder carcinoma; cancer cell culture; cancer resistance; cytotoxicity; drug sensitivity; drug targeting; human; human cell; pharmacogenetics; priority journal; promoter region; protein expression; protein function; transactivation; transcription regulation; tumor suppressor gene; upregulation; Apoptosis; CCAAT-Enhancer-Binding Protein-delta; Cell Line, Transformed; Cell Line, Tumor; Cisplatin; Drug Delivery Systems; Drug Resistance, Neoplasm; Humans; Superoxide Dismutase; Transcription, Genetic; Transcriptional Activation; Up-Regulation; Urologic Neoplasms |
顯示於: | 醫學系 |
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