Journal
CANCER CELL
Volume 24, Issue 5, Pages 603-616Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2013.10.003
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Funding
- 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
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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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