低氧和自噬与肿瘤的发生发展  

Hypoxia and autophagy and their correlation with tumorigenesis and development

作　　者：陈冠辉[1,2] 侯劲松[1,2] 

机构地区：[1]中山大学光华口腔医学院.附属口腔医院口腔颌面外科 [2]广东省口腔医学重点实验室,广州510055

出　　处：《国际口腔医学杂志》2016年第5期584-588,共5页International Journal of Stomatology

基　　金：广东省自然科学基金(10151008901000025);广东省科技计划项目(2013B021800059);广州市科信局对外科技合作计划项目(2012J5100008)~~

摘　　要：自噬作为真核生物的一种应激调控机制,既可以促进肿瘤的发生发展,又可以抑制肿瘤的增殖。在肿瘤局部低氧的微环境下,低氧诱导因子-1α、哺乳动物雷帕霉素靶蛋白信号转导通路抑制、内质网应激均可促进自噬的发生。在肿瘤快速地发生发展过程中,肿瘤的糖代谢功能增强、活性氧族增多、窖蛋白1下调以及上皮间质转化的激活均诱导了自噬的发生并促进肿瘤的局部浸润、侵袭转移和耐药,因此,抑制自噬可能为肿瘤治疗提供一种新的策略。Autophagy is a stress regulatory mechanism that generally exists in eukaryotic cells. This process promotes tumor development and inhibits tumor proliferation. Autophagy is activated by increasing hypoxia inducible factor-1 ct level, suppressing the mammalian target of the rapamycin signal pathway, and inducing endoplasmic reticulum stress in the tumor hypoxia microenvironment. Autophagy is stimulated through enhancement of glucose metabolism, increase in reactive oxygen species level, downregulation of caveolin 1 expression, and activation of epithelial-mesenchymal transition in tumor during rapid cell proliferation and invasion. Autophagy promotes tumor invasion, metastasis, and drug resistance. Therefore, novel strategies for inhibiting autophagy may serve as promising therapeutic approach for tumor treatment.

关 键 词：低氧 自噬 肿瘤 

分 类 号：R730.2[医药卫生—肿瘤]