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细胞凋亡与自噬相互作用的新见解

Novel Insights into the Interplay between Apoptosis and Autophagy.

作者信息

Rikiishi Hidemi

机构信息

Department of Microbiology and Immunology, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.

出版信息

Int J Cell Biol. 2012;2012:317645. doi: 10.1155/2012/317645. Epub 2012 Mar 15.

DOI:10.1155/2012/317645
PMID:22496691
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3312193/
Abstract

For several decades, apoptosis has taken center stage as the principal mechanism of programmed cell death (type I cell death) in mammalian tissues. Autophagic cell death (type II) is characterized by the massive accumulation of autophagic vacuoles in the cytoplasm of cells. The autophagic process is activated as an adaptive response to a variety of extracellular and intracellular stresses, including nutrient deprivation, hormonal or therapeutic treatment, pathogenic infection, aggregated and misfolded proteins, and damaged organelles. Increasing evidence indicates that autophagy is associated with a number of pathological processes, including cancer. The regulation of autophagy in cancer cells is complex since it can enhance cancer cell survival in response to certain stresses, while it can also act to suppress the initiation of cancer growth. This paper focused on recent advances regarding autophagy in cancer and the techniques currently available to manipulate autophagy.

摘要

几十年来,细胞凋亡一直是哺乳动物组织中程序性细胞死亡(I型细胞死亡)的主要机制。自噬性细胞死亡(II型)的特征是细胞胞质中自噬泡大量积累。自噬过程作为对多种细胞外和细胞内应激的适应性反应而被激活,这些应激包括营养剥夺、激素或治疗处理、病原体感染、聚集和错误折叠的蛋白质以及受损的细胞器。越来越多的证据表明自噬与包括癌症在内的许多病理过程相关。癌细胞中自噬的调节很复杂,因为它在应对某些应激时可增强癌细胞的存活能力,而同时它也可能抑制癌症生长的起始。本文重点关注了癌症中自噬的最新进展以及目前可用于调控自噬的技术。

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本文引用的文献

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Targeting autophagy enhances sorafenib lethality for hepatocellular carcinoma via ER stress-related apoptosis.靶向自噬通过内质网应激相关凋亡增强索拉非尼对肝癌的致死作用。
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