细胞凋亡——助长致癌之火。

IF 5.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
FEBS Journal Pub Date : 2021-08-01 Epub Date: 2020-11-25 DOI:10.1111/febs.15624
Camila Castillo Ferrer, Kevin Berthenet, Gabriel Ichim
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引用次数: 32

摘要

细胞凋亡是研究最广泛的程序性细胞死亡形式,对机体稳态至关重要。凋亡细胞死亡已被广泛报道为一种肿瘤抑制机制。然而,最近的研究表明,细胞凋亡发挥非经典功能,并可能矛盾地促进肿瘤生长和转移。癌症细胞对凋亡的劫持可能在不同水平上发生,要么是通过凋亡细胞与其局部或远处微环境的相互作用,要么是主要凋亡效应子(即胱天蛋白酶和线粒体)的异常促神经作用,特别是在凋亡失败时。在这篇综述中,我们强调了一些最近描述的凋亡和这些效应物可能促进癌症侵袭性的机制。我们认为,更好地理解细胞凋亡的非经典作用可能对开发更有效的癌症疗法至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Apoptosis - Fueling the oncogenic fire.

Apoptosis - Fueling the oncogenic fire.

Apoptosis - Fueling the oncogenic fire.

Apoptosis - Fueling the oncogenic fire.
Apoptosis, the most extensively studied form of programmed cell death, is essential for organismal homeostasis. Apoptotic cell death has widely been reported as a tumor suppressor mechanism. However, recent studies have shown that apoptosis exerts noncanonical functions and may paradoxically promote tumor growth and metastasis. The hijacking of apoptosis by cancer cells may arise at different levels, either via the interaction of apoptotic cells with their local or distant microenvironment, or through the abnormal pro‐oncogenic roles of the main apoptosis effectors, namely caspases and mitochondria, particularly upon failed apoptosis. In this review, we highlight some of the recently described mechanisms by which apoptosis and these effectors may promote cancer aggressiveness. We believe that a better understanding of the noncanonical roles of apoptosis may be crucial for developing more efficient cancer therapies.
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来源期刊
FEBS Journal
FEBS Journal 生物-生化与分子生物学
CiteScore
11.70
自引率
1.90%
发文量
375
审稿时长
1 months
期刊介绍: The FEBS Journal is an international journal devoted to the rapid publication of full-length papers covering a wide range of topics in any area of the molecular life sciences. The criteria for acceptance are originality and high quality research, which will provide novel perspectives in a specific area of research, and will be of interest to our broad readership. The journal does not accept papers that describe the expression of specific genes and proteins or test the effect of a drug or reagent, without presenting any biological significance. Papers describing bioinformatics, modelling or structural studies of specific systems or molecules should include experimental data.
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