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自噬在病毒发展及癌症进展中的作用

Autophagy in Viral Development and Progression of Cancer.

作者信息

Suares Alejandra, Medina María Victoria, Coso Omar

机构信息

Departamento de Fisiología y Biología Molecular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.

Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), CONICET-Universidad de Buenos Aires, Buenos Aires, Argentina.

出版信息

Front Oncol. 2021 Mar 8;11:603224. doi: 10.3389/fonc.2021.603224. eCollection 2021.

DOI:10.3389/fonc.2021.603224
PMID:33763351
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7982729/
Abstract

Autophagy is a complex degradative process by which eukaryotic cells capture cytoplasmic components for subsequent degradation through lysosomal hydrolases. Although this catabolic process can be triggered by a great variety of stimuli, action in cells varies according to cellular context. Autophagy has been previously linked to disease development modulation, including cancer. Autophagy helps suppress cancer cell advancement in tumor transformation early stages, while promoting proliferation and metastasis in advanced settings. Oncoviruses are a particular type of virus that directly contribute to cell transformation and tumor development. Extensive molecular studies have revealed complex ways in which autophagy can suppress or improve oncovirus fitness while still regulating viral replication and determining host cell fate. This review includes recent advances in autophagic cellular function and emphasizes its antagonistic role in cancer cells.

摘要

自噬是一个复杂的降解过程,真核细胞通过该过程捕获细胞质成分,以便随后通过溶酶体水解酶进行降解。尽管这个分解代谢过程可以由各种各样的刺激触发,但在细胞中的作用会因细胞环境而异。自噬此前已与包括癌症在内的疾病发展调节相关联。自噬在肿瘤转化的早期阶段有助于抑制癌细胞进展,而在晚期则促进增殖和转移。致癌病毒是一类特殊的病毒,直接促成细胞转化和肿瘤发展。广泛的分子研究揭示了自噬抑制或提高致癌病毒适应性的复杂方式,同时仍调节病毒复制并决定宿主细胞命运。这篇综述包括自噬细胞功能的最新进展,并强调其在癌细胞中的拮抗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/29d1c015d143/fonc-11-603224-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/3000e3c2ccdd/fonc-11-603224-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/8590cee9e17c/fonc-11-603224-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/2a623063db59/fonc-11-603224-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/909ae3033f72/fonc-11-603224-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/2a2a821d8a8d/fonc-11-603224-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/f95eb3f5c326/fonc-11-603224-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/29d1c015d143/fonc-11-603224-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/3000e3c2ccdd/fonc-11-603224-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/8590cee9e17c/fonc-11-603224-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/2a623063db59/fonc-11-603224-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/909ae3033f72/fonc-11-603224-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/2a2a821d8a8d/fonc-11-603224-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/f95eb3f5c326/fonc-11-603224-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00fc/7982729/29d1c015d143/fonc-11-603224-g007.jpg

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