Growth arrest induced by C75, a fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma
文献类型：期刊论文
| 作者 | Gao, Yan; Lin, Li-Ping; Zhu, Cai-Hua; Chen, Yi ; Hou, Yong-Tai; Ding, Jian
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| 刊名 | CANCER BIOLOGY & THERAPY
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| 出版日期 | 2006-08 |
| 卷号 | 5期号:8页码:978-985 |
| 关键词 | C75 fatty acid synthase hepatocellular carcinoma cell cycle arrest p38 MAPK p53 RNA interference |
| ISSN号 | 1538-4047 |
| DOI | 10.4161/cbt.5.8.2883 |
| 文献子类 | Article |
| 英文摘要 | C75, a well-known fatty acid synthase (FAS) inhibitor, has been shown to possess potent anti-cancer activity in vitro and in vivo. In this study, we reveal that C75 is a cell cycle arrest inducer and explore the potential mechanisms for this effect in hepatocellular carcinoma (HCC) cell lines with abundant FAS expression: HepG2 and SMMC7721 cells with wt-p53, and Hep3B cells with null p53. The results showed FAS protein expression and basal activity levels were higher in HepG2 cells than in the other two HCC cell lines. Treatment with C75 inhibited FAS activity within 30 min of administration and induced G(2) phase arrest accompanied by p53 overexpression in HepG2 and SMMC7721 cells. By contrast, C75 triggered G(1) phase arrest in Hep3B cells, and RNA interference targeting p53 did not attenuate C75-induced G(2) arrest in HepG2 cells. Similarly, p53 overexpression via p53 plasmid transfection did not affect C75-induced G, phase arrest in Hep3B cells. However, we observed a clear correlation between p38 MAPK activation triggered by C75 and the induction of cell cycle arrest in all three HCC cells. Furthermore, treatment with the p38 MAPK inhibitor SB203580 reduced p38 MAPK activity and cell cycle arrest, and also partially restored cyclin A, cyclin B1, cyclin D1 and p21 protein levels. Collectively, it was p38 MAPK but not p53 involved in C75-mediated tumor cell growth arrest in HCC cells. |
| WOS关键词 | ACTIVATED PROTEIN-KINASES ; CELL-CYCLE ARREST ; BREAST-CANCER ; EXPRESSION ; APOPTOSIS ; FAS ; OVEREXPRESSION ; PROLIFERATION ; ONCOGENE ; SURVIVAL |
| WOS研究方向 | Oncology |
| 语种 | 英语 |
| WOS记录号 | WOS:000242400700023 |
| 出版者 | LANDES BIOSCIENCE |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/273524]  |
| 专题 | 成果转移转化处 中科院受体结构与功能重点实验室 新药研究国家重点实验室 药理学第一研究室 科研与新药推进处 |
| 通讯作者 | Lin, Li-Ping |
| 作者单位 | Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai Inst Biol Sci,Div Antitumor Pharmacol, State Key Lab Drug Res, Shanghai 201203, Peoples R China |
| 推荐引用方式 GB/T 7714 | Gao, Yan,Lin, Li-Ping,Zhu, Cai-Hua,et al. Growth arrest induced by C75, a fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma[J]. CANCER BIOLOGY & THERAPY,2006,5(8):978-985. |
| APA | Gao, Yan,Lin, Li-Ping,Zhu, Cai-Hua,Chen, Yi,Hou, Yong-Tai,&Ding, Jian.(2006).Growth arrest induced by C75, a fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma.CANCER BIOLOGY & THERAPY,5(8),978-985. |
| MLA | Gao, Yan,et al."Growth arrest induced by C75, a fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma".CANCER BIOLOGY & THERAPY 5.8(2006):978-985. |
入库方式： OAI收割
来源：上海药物研究所
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