期刊
CANCER CELL
卷 24, 期 5, 页码 603-616出版社
CELL PRESS
DOI: 10.1016/j.ccr.2013.10.003
关键词
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资金
- Korea Science and Engineering Foundation [R16-2003-002-01001-02006]
- Cooperative Research Program for Agriculture Science and Technology Development of Korea [PJ009507]
- National Research Foundation of Korea [NRF-2007-0054930]
- Cancer Science Institute, National University of Singapore
- Translational and Clinical Research (TCR) Flagship program grant (The Singapore Gastric Cancer Consortium) from the National Medical Research Council, Singapore
Targeted inactivation of Runx3 in mouse lung induced mucinous and nonmucinous adenomas and markedly shortened latency of adenocarcinoma formation induced by oncogenic K-Ras. RUNX3 was frequently inactivated in K-RAS mutated human lung adenocarcinomas. A functional genetic screen of a fly mutant library and molecular analysis in cultured cell lines revealed that Runx3 forms a complex with BRD2 in a K-Ras-dependent manner in the early phase of the cell cycle; this complex induces expression of p14(ARF)/p19(Arf) and p21(WAF/CIP). When K-Ras was constitutively activated, the Runx3-BRD2 complex was stably maintained and expression of both p14(ARF) and p21(WAF/CIP) was prolonged. These results provide a missing link between oncogenic K-Ras and the p14(ARF)-p53 pathway, and may explain how cells defend against oncogenic K-Ras.
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