Non-genomic loss of PTEN function in cancer: not in my genes

被引：124

作者：

Leslie, Nick R. ^{[1
]}

Foti, Michelangelo ^{[2
]}

机构：

[1] Univ Dundee, Coll Life Sci, Div Mol Physiol, Wellcome Trust Bioctr, Dundee DD1 5EH, Scotland

[2] Univ Geneva, Geneva Med Fac, Ctr Med Univ, Dept Cellular Physiol & Metab, CH-1211 Geneva 4, Switzerland

来源：

TRENDS IN PHARMACOLOGICAL SCIENCES | 2011年 / 32卷 / 03期

基金：

英国医学研究理事会; 瑞士国家科学基金会;

关键词：

TUMOR-SUPPRESSOR PTEN; TENSIN-HOMOLOG PTEN; PROTEIN-KINASE CK2; UP-REGULATION; DOWN-REGULATION; CELL-SURVIVAL; PPAR-GAMMA; UBIQUITIN LIGASE; REDOX REGULATION; MICROSATELLITE INSTABILITY;

D O I：

10.1016/j.tips.2010.12.005

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Loss of function of the phosphatase and tensin homolog (PTEN) tumour suppressor contributes to the development of many cancers. However, in contrast to classical models of tumour suppression, partial loss of PTEN function appears to be frequently observed in the clinic. In addition, studies of both humans and mice with reductions in PTEN gene dosage indicate that even partial loss of PTEN function is sufficient to promote some cancer types, particularly in the breast. PTEN expression appears to be tightly controlled both transcriptionally and post-transcriptionally, with several recent studies implicating oncogenic microRNAs in PTEN suppression. The lipid phosphatase activity of PTEN can also be regulated post-translationally via inhibitory phosphorylation, ubiquitination or oxidation. Here we discuss these multiple mechanisms of PTEN regulation. We also put into context recent proposals that changes in this regulation can drive tumour development and address the accompanying evidence for their clinical significance.

引用

页码：131 / 140

页数：10

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