Interplay between ROS and autophagy in cancer cells, from tumor initiation to cancer therapy

被引:381
|
作者
Poillet-Perez, Laura [1 ]
Despouy, Gilles [1 ]
Delage-Mourroux, Regis [1 ]
Boyer-Guittaut, Michael [1 ]
机构
[1] Univ Franche Comte, Biochim Lab, Estrogenes Express Gen & Pathol Syst Nerveux Cent, UFR Sci & Tech,SFR IBCT FED4234, F-25030 Besancon, France
来源
REDOX BIOLOGY | 2015年 / 4卷
关键词
ROS; Mitochondria; Antioxidant; Mitophagy; Autophagy; Cancer; ACTIVATED PROTEIN-KINASE; KAPPA-B ACTIVATION; OXIDATIVE STRESS; MITOCHONDRIAL AUTOPHAGY; STROMA COEVOLUTION; METABOLISM; HYPOXIA; GROWTH; METASTASIS; MECHANISMS;
D O I
10.1016/j.redox.2014.12.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cancer formation is a complex and highly regulated multi step process which is highly dependent of its environment, from the tissue to the patient. This complexity implies the development of specific treatments adapted to each type or tumor. The initial step or cancer formation requires the transformation of a healthy cell to a cancer cell, a process regulated by multiple intracellular and extracellular stimuli. The further steps, from the anarchic proliferation of cancer cells to form a primary tumor to the migration of cancer cells to distant organs to form metastasis, are also highly dependent of the tumor environment but of intracellular molecules and pathways as well. In this review, we will focus on the regulatory role of reactive oxygen species (ROS) and autophagy levels during the course of cancer development, from cellular transformation to the formation of metastasis. These data will allow us to discuss the potential of this molecule or pathway as putative future therapeutic targets. (C) 2014 The Authors. Published by Elsevier B.V.
引用
收藏
页码:184 / 192
页数:9
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