HSF1 blockade-induced tumor thermotolerance abolishment is mediated by JNK-dependent caspase-3 activation

Biochemical and Biophysical Research Communications
Jin-Hui WangXin-Yuan Liu

Abstract

We previously blocked the heat shock transcription factor 1 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 t...Continue Reading

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Citations

Mar 11, 2006·Apoptosis : an International Journal on Programmed Cell Death·M LauricellaG Tesoriere
May 13, 2010·Journal of Translational Medicine·Cheng WangGuangxiu Lu
Feb 3, 2009·Journal of Hematology & Oncology·Mark G Goldstein, Zihai Li
Jan 18, 2013·World Journal of Gastroenterology : WJG·Feng XiaoQing-Xian Zhu
Feb 22, 2005·Biochemical and Biophysical Research Communications·Shigenori HoshinoIchiro Kawase
May 10, 2005·Journal of Pharmacological Sciences·Takayuki SakaiMitsuru Kawaguchi

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