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翻译机制对自噬的调控及其在癌症中的意义

Autophagy Regulation by the Translation Machinery and Its Implications in Cancer.

作者信息

Acevo-Rodríguez Pilar Sarah, Maldonado Giovanna, Castro-Obregón Susana, Hernández Greco

机构信息

PSA-R and SC-O, División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico.

Translation and Cancer Laboratory, Unit of Biomedical Research on Cancer, National Institute of Cancer (Instituto Nacional de Cancerología, INCan), Mexico City, Mexico.

出版信息

Front Oncol. 2020 Mar 13;10:322. doi: 10.3389/fonc.2020.00322. eCollection 2020.

DOI:10.3389/fonc.2020.00322
PMID:32232004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7082396/
Abstract

Various metabolic pathways and molecular processes in the cell act intertwined, and dysregulating the interplay between some of them may lead to cancer. It is only recently that defects in the translation process, i.e., the synthesis of proteins by the ribosome using a messenger (m)RNA as a template and translation factors, have begun to gain strong attention as a cause of autophagy dysregulation with effects in different maladies, including cancer. Autophagy is an evolutionarily conserved catabolic process that degrades cytoplasmic elements in lysosomes. It maintains cellular homeostasis and preserves cell viability under various stress conditions, which is crucial for all eukaryotic cells. In this review, we discuss recent advances shedding light on the crosstalk between the translation and the autophagy machineries and its impact on tumorigenesis. We also summarize how this interaction is being the target for novel therapies to treat cancer.

摘要

细胞内的各种代谢途径和分子过程相互交织,其中一些途径之间的相互作用失调可能导致癌症。直到最近,翻译过程中的缺陷,即核糖体以信使核糖核酸(mRNA)为模板并利用翻译因子合成蛋白质的过程,才开始作为自噬失调的一个原因而受到强烈关注,这种失调会在包括癌症在内的不同疾病中产生影响。自噬是一种进化上保守的分解代谢过程,它在溶酶体中降解细胞质成分。它维持细胞内稳态,并在各种应激条件下保持细胞活力,这对所有真核细胞都至关重要。在这篇综述中,我们讨论了最近在翻译和自噬机制之间的相互作用及其对肿瘤发生的影响方面取得的进展。我们还总结了这种相互作用如何成为治疗癌症的新型疗法的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/8f30cbd67760/fonc-10-00322-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/0e6a5114bb8d/fonc-10-00322-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/187e39ae166e/fonc-10-00322-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/33d66dc250f0/fonc-10-00322-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/3735d81fac7b/fonc-10-00322-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/8f30cbd67760/fonc-10-00322-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/0e6a5114bb8d/fonc-10-00322-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/187e39ae166e/fonc-10-00322-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/33d66dc250f0/fonc-10-00322-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/3735d81fac7b/fonc-10-00322-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11c5/7082396/8f30cbd67760/fonc-10-00322-g0005.jpg

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