PTEN Mouse Models of Cancer Initiation and and Progression

被引：25

作者：

Lee, Yu-Ru ^{[1
]}

Pandolfi, Pier Paolo ^{[1
]}

机构：

[1] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med & Pathol, Canc Res Inst,Beth Israel Deaconess Canc Ctr, Boston, MA 02215 USA

来源：

COLD SPRING HARBOR PERSPECTIVES IN MEDICINE | 2020年 / 10卷 / 02期

关键词：

PROSTATE-CANCER; CELLULAR SENESCENCE; SUPPRESSOR GENE; NUCLEAR IMPORT; TUMOR; MUTATION; ACTIVATION; PHOSPHATASE; METASTASIS; EXPRESSION;

D O I：

10.1101/cshperspect.a037283

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is one of the most frequently mutated, deleted, and functionally inactivated tumor suppressor genes in human cancer. PTEN is found mutated both somatically and in the germline of patients with PTEN hamartoma tumor syndrome (PHTS). PTEN encodes a dual lipid and protein phosphatase that dephosphorylates the lipid phosphatidylinositol-3,4,5-trisphosphate (PIP3), in turn negatively regulating the oncogenic PI3K-AKT pathway, a key proto-oncogenic player in cancer development and progression. Because of importance of PTEN in tumorigenesis, a large number of sophisticated genetically engineered mouse models (GEMMs) has been designed to elucidate the underlying mechanisms by which the "PTEN pathway" promotes tumorigenesis, while simultaneously providing a well-tailored system for the identification of novel therapies and offering platforms for new drug discoveries. This review summarizes the major cancer mouse models through which the PTEN pathway has been genetically deconstructed, and outlines the rapid development of GEMMs toward more detailed functional and tissue-specific analysis.

引用

页数：12

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