The functions and regulation of the PTEN tumour suppressor

被引:1544
|
作者
Song, Min Sup [1 ]
Salmena, Leonardo [1 ,2 ]
Pandolfi, Pier Paolo [1 ]
机构
[1] Harvard Univ, Sch Med, Dept Pathol & Med, Beth Israel Deaconess Canc Ctr,Canc Genet Program, Boston, MA 02215 USA
[2] Univ Hlth Network, Ontario Canc Inst, Princess Margaret Hosp, Toronto, ON M5G 2M9, Canada
基金
美国国家卫生研究院; 加拿大健康研究院;
关键词
HEMATOPOIETIC STEM-CELLS; TENSIN-HOMOLOG PTEN; PROSTATE-CANCER; NEGATIVE REGULATION; PATHWAY ACTIVATION; GENETIC DISSECTION; UBIQUITIN LIGASE; NUCLEAR PTEN; MOUSE MODEL; SOMA SIZE;
D O I
10.1038/nrm3330
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The importance of the physiological function of phosphatase and tensin homologue (PTEN) is illustrated by its frequent disruption in cancer. By suppressing the phosphoinositide 3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathway through its lipid phosphatase activity, PTEN governs a plethora of cellular processes including survival, proliferation, energy metabolism and cellular architecture. Consequently, mechanisms regulating PTEN expression and function, including transcriptional regulation, post-transcriptional regulation by non-coding RNAs, post-translational modifications and protein-protein interactions, are all altered in cancer. The repertoire of PTEN functions has recently been expanded to include phosphatase-independent activities and crucial functions within the nucleus. Our increasing knowledge of PTEN and pathologies in which its function is altered will undoubtedly inform the rational design of novel therapies.
引用
收藏
页码:283 / 296
页数:14
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