| First Author | Lee YS | Year | 2013 |
| Journal | Cancer Cell | Volume | 24 |
| Issue | 5 | Pages | 603-16 |
| PubMed ID | 24229708 | Mgi Jnum | J:206737 |
| Mgi Id | MGI:5551925 | Doi | 10.1016/j.ccr.2013.10.003 |
| Citation | Lee YS, et al. (2013) Runx3 inactivation is a crucial early event in the development of lung adenocarcinoma. Cancer Cell 24(5):603-16 |
| abstractText | 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. |
