期刊
CANCER LETTERS
卷 275, 期 2, 页码 221-226出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2008.10.018
关键词
Proliferation; NM23; NM23H2; Metastasis; ERK; Ras; Signal transduction; The Ras-ERK pathway
类别
资金
- National Research Laboratory
- Korea Science and Engineering Foundation (KOSEF) [2005-01564, 2006-02681, R112000078010020, 2007-000-10004-0]
- Ministry of Education and Human Resources Development
- National Research Foundation of Korea [2005-01564, 2006-02681] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The NM23 family proteins are involved in a variety of biological processes including tumor metastasis, development, and differentiation; however, their functions in the regulation of cellular proliferation are poorly understood. We have investigated the role of one NM23 family protein, NM23H2, in the regulation of cellular proliferation directed by the extracellular signal regulated kinase (ERK) pathway. The activity of ERKs was enhanced by knockdown of endogenous NM23H2 and blocked by overexpression of NM23H2 in both NIH3T3 and HEK293 cells. Additionally, the epidermal growth factor (EGF)- and oncogenic Ras(G12R)-induced proliferation of both HEK293 and NIH3T3 cells was reduced by NM23H2 overexpression. Furthermore, activation of Raf-1, MEK and the ERKs by either EGF or Ras(G12R) was inhibited by NM23H2 overexpression. Together, our data indicate that NM23H2 is a negative regulator of cellular proliferation stimulated by EGF- and Ras-mediated activation of the ERK pathway. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据