ERK1/2 activation plays important roles in the opposite effects of Trichostatin A in non-cancer and cancer cells | |
Zhang Y1,2; Yu GY1,3; Wang DM4; Hu Y4; Lei WW[*]1,4 | |
刊名 | TOXICON |
2011 | |
卷号 | 57期号:6页码:932-937 |
关键词 | HDAC inhibitor TSA Apoptosis ERK1/2 |
通讯作者 | leiweiwei@kmust.edu.cn |
合作状况 | 其它 |
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. |
收录类别 | SCI |
资助信息 | This work was supported by The National Natural Science Foundation of China(30730023,30721065,30623003)andtheNational Basic Research Program of China (2007CB947900). |
语种 | 英语 |
公开日期 | 2011-06-13 |
内容类型 | 期刊论文 |
源URL | [http://159.226.149.42:8088/handle/353002/6622] |
专题 | 昆明动物研究所_动物活性蛋白多肽组学 昆明动物研究所_动物模型与人类重大疾病机理重点实验室 |
作者单位 | 1.Laboratory of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Kunming University of Science and Technology, 296 Bailongsi Road, Kunming 650224, China 2.Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China 3.Department of Biochemistry, Kunming Medical College, Kunming, Yunnan 650032, China 4.Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China |
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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