内质网应激/未折叠蛋白反应促进肿瘤侵袭的研究进展  

Advances of Endoplasmic Reticulum Stress/Unfolded Protein Response Promote Tumor Invasion

作　　者：于涛[1] 柴双 欧阳仲瑞 刘耀华[1] 

机构地区：[1]哈尔滨医科大学附属第一医院神经外科,哈尔滨150001 [2]内蒙古扎兰屯中蒙医院神经外科,扎兰屯162650

出　　处：《肿瘤防治研究》2017年第4期298-302,共5页Cancer Research on Prevention and Treatment

基　　金：国家自然科学基金(81372701)

摘　　要：内质网应激/未折叠蛋白反应促进肿瘤侵袭是肿瘤调控的新机制,适度的内质网应激不仅可以保护细胞还能促进肿瘤细胞侵袭。许多研究表明内质网应激/未折叠蛋白反应与肿瘤的发生发展密切相关,且能通过上调血管内皮生长因子、葡萄糖调节蛋白78、前梯度蛋白2的表达、促进上皮间质转化、降解细胞外基质等方式促进肿瘤侵袭,了解内质网应激/未折叠蛋白反应与肿瘤侵袭性之间的关系可能为肿瘤治疗提供新方向。本文将对内质网应激/未折叠蛋白反应促进肿瘤侵袭的相关机制作一综述。Endoplasmic reticulum stress/unfolded protein response is a new regulatory mechanism that promote tumor invasion. Moderate endoplasmic reticulum stress can not only protect the cells but also promote cell invasive. Many studies have shown that endoplasmic reticulum stress/unfolded proteins response is closely related to the development of tumor and can promote tumor invasion through regulate the expression of the Vascular endothelial growth factor（VEGF）, glucose-regulated protein78（GRP78）, anterior gradient 2（AGR2）, promote the transformation of epithelial mesenchymal and degrade extracellular matrix. Understand the links between endoplasmic reticulum stress/unfolded protein response and tumor invasion may provide a new direction for tumor treatment. In this article, we will review summarize the current knowledge about the relevant mechanism of endoplasmic reticulum stress/unfolded proteins response promote tumor invasion.

关 键 词：内质网应激 侵袭 血管内皮生长因子 上皮间质转化 葡萄糖调节蛋78 前梯度蛋白2 细胞外基质 

分 类 号：R730[医药卫生—肿瘤]