ERK1/2 activation plays important roles in the opposite effects of Trichostatin A in non-cancer and cancer cells
文献类型：期刊论文
| 作者 | Zhang, Y; Yu, GY; Wang, DM; Hu, Y; Lei, WW |
| 刊名 | TOXICON
 |
| 出版日期 | 2011 |
| 卷号 | 57期号:6页码:932-937 |
| 关键词 | HDAC inhibitor TSA Apoptosis ERK1/2 Non-cancer cells Cancer cells |
| 通讯作者 | Lei, WW (reprint author), Kunming Univ Sci & Technol, Lab Mol Genet Aging & Tumor, Fac Life Sci & Technol, 296 Bailongsi Rd, Kunming 650224, Peoples R China.,leiweiwei@kmust.edu.cn |
| 英文摘要 | Histone deacetylase (HDAC) inhibitors are candidates of anti-cancer drugs as they can effectively kill cancer cells while have little or no toxicity to non-cancer cells, but the molecular mechanism underlying this process remains unclear. We previously reported that HDAC inhibitors could protect normal mouse hepatocytes from apoptosis induced by transforming growth factor-beta 1 (TGF-beta 1) with the requirement of extracellular signal-regulated kinase 1/2 (ERK1/2). In this study, we investigate the roles of trichostatin A (TSA), a typical HDAC inhibitor, on three non-cancer cell lines AML-12, MDCK and 3T3-L1, and four cancer cell lines Hep-3B, HeLa, A549 and MCF-7. TSA is a fermentation product of Streptomyces originally used as an antifungal agent. Our results showed that TSA blocked not only the TGF-beta 1-induced apoptosis but also serum starvation-induced apoptosis in all the non-cancer cells, whereas it could induce strong apoptosis in all the cancer cells. Further investigation revealed that TSA can induce the activation of ERK1/2 in the three non-cancer cells but not in the cancer cells. In summary, these findings indicated that TSA protect non-cancer cells from apoptosis via activating ERK1/2, providing a useful insight into the better application of HDAC inhibitors in cancer therapy. (C) 2011 Elsevier Ltd. All rights reserved. |
| 学科主题 | Pharmacology & Pharmacy; Toxicology |
| 类目[WOS] | Pharmacology & Pharmacy ; Toxicology |
| 关键词[WOS] | HISTONE-DEACETYLASE INHIBITORS ; HEPATOMA-CELLS ; APOPTOSIS ; GROWTH ; OSTEOSARCOMA ; SPECIFICITY ; TRANSITION ; MECHANISMS ; SURVIVAL ; THERAPY |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000290696900014 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/827]  |
| 专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
| 推荐引用方式 GB/T 7714 | Zhang, Y,Yu, GY,Wang, DM,et al. ERK1/2 activation plays important roles in the opposite effects of Trichostatin A in non-cancer and cancer cells[J]. TOXICON,2011,57(6):932-937. |
| APA | Zhang, Y,Yu, GY,Wang, DM,Hu, Y,&Lei, WW.(2011).ERK1/2 activation plays important roles in the opposite effects of Trichostatin A in non-cancer and cancer cells.TOXICON,57(6),932-937. |
| MLA | Zhang, Y,et al."ERK1/2 activation plays important roles in the opposite effects of Trichostatin A in non-cancer and cancer cells".TOXICON 57.6(2011):932-937. |
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