摘要
了解调节内质网应激反应诱导肿瘤细胞凋亡的研究进展.通过对国内外有关内质网应激反应诱导肿瘤细胞凋亡的文献进行综述.未折叠或折叠错误的蛋白质在内质网(endoplasmic reticulum ER)上过度积累,导致内质网产生应激反应从而激活保护细胞的信号通路,通常称为未折叠蛋白反应(unfolded protein response UPR).如果内质网受到的刺激不减弱,UPR反应会恢复和保持内质网上的动态平衡或者诱导细胞凋亡.UPR反应的信号网络包含三个核心要素,分别为肌醇需要酶1(inositol-requiring protein-1 IRE1)、PFR样内质网激酶(PKR-like ER kinase PERK)和转录活化因子6(activating transcription factor 6 ATF6).在肿瘤细胞内质网应激反应中,如何调节其反应通路因子使得三种信号通路协同或者单一的诱导肿瘤细胞凋亡仍需进一步研究.
In order to review the advances of endoplasmic reticulum stress response induce the apoptosis of tumor cells , this paper summarized litertures about endoplasmic reticulum stress response induced the apoptosis of tumor cells .Unfolded or misfolded proteins accumu-late excessively in the endoplasmic reticulum ,leading endoplasmic reticulum stress response to activate the signaling pathways of protecting cells , which commonly called unfolded pro-tein response （ UPR） .If the endoplasmic reticulum was not reduced stimulation , UPR re-sponse will be restore and maintain the homeostasis of endoplasmic reticulum or induce apop -tosis.The signal net of UPR contains three core elements： inositol -requiring protein -1 （IRE1）,PKR-like ER kinase PERK and activating transcription factor 6（ ATF6）.In the endoplasmic reticulum stress response of tumor cells , how to adjust the reaction pathway fac-tor makes three kinds of signaling pathway induced apoptosis in tumor cells jointly or single requires further research .
出处
《哈尔滨商业大学学报（自然科学版）》
CAS
2014年第1期21-24,共4页
Journal of Harbin University of Commerce：Natural Sciences Edition
基金
国家自然科学基金(81274067)
黑龙江省自然科学基金(D201126)
黑龙江省教育厅科技项目(1211135)
教育部科学技术研究重点项目(211045)
教育部博士点基金项目(20112332110003)
黑龙江省教育厅科技重点项目(12511z011)
黑龙江省研究生创新基金项目(YJSCX2011-165HLJ)
哈尔滨市青年科技创新人才专项资金(2013RFQXJ150)
关键词
细胞凋亡
内质网应激
内质网途径
cell apoptosis
endoplasmic reticulum stress
pathway of endoplasmic reticulum
