AKT-p53 axis protect cancer cells from autophagic cell death during nutrition deprivation

被引：6
|
作者：
Sudhagar, S. [1 ]
Sathya, S. [1 ]
Gokulapriya, G. [1 ]
Lakshmi, B. S. [1 ,2 ]
机构：
[1] Anna Univ, Dept Biotechnol, Ctr Biotechnol, Madras 600025, Tamil Nadu, India
[2] Anna Univ, Dept Biotechnol, Ctr Food Technol, Madras 600025, Tamil Nadu, India
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2016年 / 471卷 / 04期
关键词：
Nutrition deprivation; AKT; p53; Autophagy; Breast cancer; SIGNALING PATHWAY; AKT; P53; AKT/PKB; MTOR; METABOLISM; ACTIVATION; SURVIVAL;
D O I：
10.1016/j.bbrc.2016.02.064
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：
An altered metabolism supports growth of tumor. AKT, a major signal integrator plays a key role in cell metabolism. We have shown that nutritional deprivation activates AKT as observed by increased phosphorylation of both Thr308 and Ser473. Pharmacological inhibition or silencing of ART by siRNA affects cell viability during starvation. The tumor suppressor, p53 is also observed to be elevated during nutritional deprivation due to ART. Silencing of ANT and p53 enhanced autophagy as evidenced by increased acidic vesicular organelles and LOB II levels, suggesting AKT-p53 to play a significant role in cell survival through regulating autophagy during nutritional deprivation. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码：396 / 401
页数：6
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