Autophagy in cellular growth control

被引:157
作者
Wang, Richard C. [2 ]
Levine, Beth [1 ,3 ,4 ]
机构
[1] Univ Texas SW Med Ctr Dallas, Div Infect Dis, Dept Internal Med, Dallas, TX 75390 USA
[2] Univ Texas SW Med Ctr Dallas, Dept Dermatol, Dallas, TX 75390 USA
[3] Univ Texas SW Med Ctr Dallas, Dept Microbiol, Dallas, TX 75390 USA
[4] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA
关键词
Autophagy; TOR signaling; Growth control; Tumorigenesis; ACTIVATED PROTEIN-KINASE; AMINO-ACID DEPRIVATION; ENDOPLASMIC-RETICULUM; MAMMALIAN TARGET; GENE-EXPRESSION; REGULATES AUTOPHAGY; SIGNALING PATHWAYS; EIF2-ALPHA KINASE; MASTER REGULATOR; DISTINCT ROLES;
D O I
10.1016/j.febslet.2010.01.009
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
Cell growth is regulated by two antagonistic processes: TOR signaling and autophagy. These processes integrate signals including growth factors, amino acids, and energy status to ensure that cell growth is appropriate to environmental conditions. Autophagy responds indirectly to the cellular milieu as a downstream inhibitory target of TOR signaling and is also directly controlled by nutrient availability, cellular energy status, and cell stress. The control of cell growth by TOR signaling and autophagy are relevant to disease, as altered regulation of either pathway results in tumorigenesis. Here we give an overview of how TOR signaling and autophagy integrate nutritional status to regulate cell growth, how these pathways are coordinately regulated, and how dysfunction of this regulation might result in tumorigenesis. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1417 / 1426
页数:10
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