PTENless means more

被引：218

作者：

Stiles, B ^{[1
]}

Groszer, M ^{[1
]}

Wang, SY ^{[1
]}

Jiao, J ^{[1
]}

Wu, H ^{[1
]}

机构：

[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA

来源：

DEVELOPMENTAL BIOLOGY | 2004年 / 273卷 / 02期

关键词：

PTEN; AKT; stem cells; organ size; migration; hormone;

D O I：

10.1016/j.ydbio.2004.06.008

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Recent studies indicate that certain key molecules that are vital for various developmental processes, such as Wnt, Shh, and Notch, cause cancer when dysregulated. PTEN, a tumor suppressor that antagonizes the PI3 kinase pathway, is the newest one on the list. The biological function of PTEN is evolutionarily conserved from C elegans to humans, and the PTEN-controlled signaling pathway regulates cellular processes crucial for normal development, including cell proliferation, soma growth, cell death, and cell migration. In this review, we will focus on the function of PTEN in murine development and its role in regulating stem cell self-renewal and proliferation. We will summarize the organomegaly phenotypes associated with Pten tissue-specific deletion and discuss how PTEN controls organ size, a fundamental aspect of development. Last, we will review the role of PTEN in hormone-dependent, adult-onset mammary and prostate gland development. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：175 / 184

页数：10

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