Cell Cycle Control by PTEN

被引:91
作者
Brandmaier, Andrew [1 ]
Hou, Sheng-Qi [1 ]
Shen, Wen H. [1 ]
机构
[1] Cornell Univ, Dept Radiat Oncol, Weill Cornell Med, New York, NY 10065 USA
基金
美国国家卫生研究院;
关键词
TUMOR-SUPPRESSOR PTEN; PROSTATE-CANCER CELLS; LIPID PHOSPHATASE-ACTIVITY; HEMATOPOIETIC STEM-CELLS; LHERMITTE-DUCLOS-DISEASE; PROTEIN-KINASE B/AKT; UBIQUITIN E3 LIGASE; TENSIN HOMOLOG PTEN; G(1) GROWTH ARREST; NUCLEAR PTEN;
D O I
10.1016/j.jmb.2017.06.004
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
Continuous and error-free chromosome inheritance through the cell cycle is essential for genomic stability and tumor suppression. However, accumulation of aberrant genetic materials often causes the cell cycle to go awry, leading to malignant transformation. In response to genotoxic stress, cells employ diverse adaptive mechanisms to halt or exit the cell cycle temporarily or permanently. The intrinsic machinery of cycling, resting, and exiting shapes the cellular response to extrinsic stimuli, whereas prevalent disruption of the cell cycle machinery in tumor cells often confers resistance to anticancer therapy. Phosphatase and tensin homolog (PTEN) is a tumor suppressor and a guardian of the genome that is frequently mutated or deleted in human cancer. Moreover, it is increasingly evident that PTEN deficiency disrupts the fundamental processes of genetic transmission. Cells lacking PTEN exhibit cell cycle deregulation and cell fate reprogramming. Here, we review the role of PTEN in regulating the key processes in and out of cell cycle to optimize genomic integrity. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:2265 / 2277
页数:13
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