HSF1 blockade-induced tumor thermotolerance abolishment is mediated by JNK-dependent caspase-3 activation
文献类型：期刊论文
| 作者 | Wang, JH; Yao, MZ; Zhang, ZL; Zhang, YH; Wang, YG; Liu, XY |
| 刊名 | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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| 出版日期 | 2004 |
| 卷号 | 321期号:3页码:736-745 |
| 关键词 | heat shock transcription factor 1 thermotolerance caspase-3 C-jun N-terminal kinase breast cancer |
| 通讯作者 | Wang, JH (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Shanghai 200031, Peoples R China.,jinhuiwang66@hotmail.com ; xyliu@sibs.ac.cn |
| 英文摘要 | We previously blocked the heat shock transcription factor I function with a dominant-negative mutant (mHSF1) in breast cancer cell line Bcap37, and found that mHSF1 sensitizes Bcap37 cells to hyperthermia by promoting the apoptotic process. Here we studied the mechanism of this abolishing process and how thermotolerance develops in Bcap37 cells. The results indicated that mHSF1 abolished acquired or intrinsic thermotolerance in Bcap37 cells by enhancing JNK and caspase-3 pathways, two stress-induced apoptotic pathways, after hyperthermia, and interference with either one of them attenuated hyperthermia-induced apoptosis. Furthermore, epistasis assay of these two pathways suggested that JNK was upstream of the caspase-3 pathway. Conversely, other hyperthermia-induced kinases implicated in cell survival and death, Akt, ERK or p38, did not influence the effect of mHSF1, indicating that these kinases were not implicated in this abolishing process. In addition, we found that the development of acquired thermotolerance of Bcap37 cells was associated with the suppression of JNK activation after mild preheat treatment and was not reduced by Akt, ERK or p38 inhibition. In contrast, the intrinsic thermotolerance of Bcap37 cells was due to the intrinsic high levels of Akt and ERK activities since Akt or ERK inhibition resulted in increased thermosensitivity of Bcap37 cells. Our results suggest that mHSF1 plays a valuable role in the thermotolerance abolishment of Bcap37 cells, which likely contributes to tumor therapy in combination with hyperthermia. (C) 2004 Elsevier Inc. All rights reserved. |
| 学科主题 | Biochemistry & Molecular Biology; Biophysics |
| 类目[WOS] | Biochemistry & Molecular Biology ; Biophysics |
| 关键词[WOS] | STRESS-INDUCED APOPTOSIS ; N-TERMINAL KINASE ; CELL-DEATH ; C-JUN ; POLY(ADP-RIBOSE) POLYMERASE ; BREAST-CANCER ; PROTEIN-KINASES ; HEAT ; HYPERTHERMIA ; TOLERANCE |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000223277600032 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/2051]  |
| 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 | Wang, JH,Yao, MZ,Zhang, ZL,et al. HSF1 blockade-induced tumor thermotolerance abolishment is mediated by JNK-dependent caspase-3 activation[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2004,321(3):736-745. |
| APA | Wang, JH,Yao, MZ,Zhang, ZL,Zhang, YH,Wang, YG,&Liu, XY.(2004).HSF1 blockade-induced tumor thermotolerance abolishment is mediated by JNK-dependent caspase-3 activation.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,321(3),736-745. |
| MLA | Wang, JH,et al."HSF1 blockade-induced tumor thermotolerance abolishment is mediated by JNK-dependent caspase-3 activation".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 321.3(2004):736-745. |
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