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首页> 外文期刊>Journal of Cellular Physiology >Nuclear clusterin accumulation during heat shock response: implications for cell survival and thermo-tolerance induction in immortalized and prostate cancer cells.
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Nuclear clusterin accumulation during heat shock response: implications for cell survival and thermo-tolerance induction in immortalized and prostate cancer cells.

机译：在热休克核clusterin积累回应:对细胞生存的影响thermo-tolerance无限增殖和诱导前列腺癌的细胞。

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摘要

Clusterin (CLU), whose role is still debated, is differentially regulated in several patho-physiological processes and invariably induced during apoptosis. In heat shock response, CLU is considered a stress-inducible, pro-survival/cyto-protective factor via an HSE element present in his promoter. In both human prostate PNT1A and PC-3 epithelial cells we found that apoptotic stimuli induced nuclear localization of CLU (nCLU), and that overexpression of nCLU is pro-apoptotic. We show here that CLU time-course accumulation kinetic is different from that of HSP70 in these cells, thus other factor(s) might mediate HSF-1 activation and CLU expression. Sub-lethal heat shock inhibited the secretion of CLU (sCLU), leading to increased cytoplasm accumulation of CLU (cCLU) in association to cell survival. At difference, lethal heat stress caused massive accumulation of pro-apoptotic nCLU in cells dying by caspase-3-dependent apoptosis. Double heat stress (sub-lethal heat shock followed by recovery and lethal stress) induced HSP70 and thermo-tolerance in PNT1A cells, but not in PC-3 cells. In PNT1A cells, CLU secretion was inhibited and cCLU was accumulated, suggesting that cCLU might be pro-survival, while in PC-3 cells accumulation of nCLU was concomitant to caspase-3 induction and PARP activation instead. Thus, CLU expression/sub-cellular localization is strictly related to cell fate. In particular, nCLU and physiological levels of HSP70 affected cell survival in an antagonistic fashion. Prevalence of heat-induced nCLU, not allowing PC-3 cells to cope with heat shock, could be the rational explaining why malignant cells are more sensitive to heat when delivered by minimally invasive procedures for ablation of localized prostate cancer.
机译：Clusterin (CLU),其作用仍争论不休,不同的监管在几个patho-physiological流程和总是诱导细胞凋亡。CLU被认为是stress-inducible,通过HSE pro-survival / cyto-protective因素元素出现在他的启动子。前列腺PNT1A曲泽上皮细胞,我们发现凋亡刺激诱导的核本地化的俱乐部(nCLU),超表达nCLU pro-apoptotic。这里CLU时间进程积累动能不同于这些细胞HSP70的如此其他因素(s)可能调解HSF-1激活和俱乐部的表情。抑制CLU (sCLU)的分泌,导致增加细胞质中积累CLU (cCLU)协会细胞生存。致命的热应力引起的大量积累pro-apoptotic nCLU在细胞死亡caspase-3-dependent细胞凋亡。剂量热休克复苏和紧随其后致命的压力)诱导HSP70和thermo-tolerance在PNT1A细胞中,但不是在曲泽细胞。细胞,CLU分泌抑制,cCLU积累,这表明cCLUpro-survival,而在曲泽细胞积累nCLU caspase-3诱导和相伴PARP激活。严格表达/亚细胞定位有关细胞的命运。生理细胞HSP70水平的影响生存在一个敌对的时尚。热nCLU越小,不允许曲泽细胞应对热休克,可能是理性的解释为什么恶性细胞更敏感当由微创热程序消融局部前列腺癌癌症。

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