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|Title:||Runx3 Inactivation Is a Crucial Early Event in the Development of Lung Adenocarcinoma||Authors:||Lee, Y.-S.
|Issue Date:||11-Nov-2013||Citation:||Lee, Y.-S., Lee, J.-W., Jang, J.-W., Chi, X.-Z., Kim, J.-H., Li, Y.-H., Kim, M.-K., Kim, D.-M., Choi, B.-S., Kim, E.-G., Chung, J.-H., Lee, O.-J., Lee, Y.-M., Suh, J.-W., Chuang, L., Ito, Y., Bae, S.-C. (2013-11-11). Runx3 Inactivation Is a Crucial Early Event in the Development of Lung Adenocarcinoma. Cancer Cell 24 (5) : 603-616. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ccr.2013.10.003||Abstract:||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 p14ARF/p19Arf and p21WAF/CIP. When K-Ras was constitutively activated, the Runx3-BRD2 complex was stably maintained and expression of both p14ARF and p21WAF/CIP was prolonged. These results provide a missing link between oncogenic K-Ras and the p14ARF-p53 pathway, and may explain how cells defend against oncogenic K-Ras. © 2013 Elsevier Inc.||Source Title:||Cancer Cell||URI:||http://scholarbank.nus.edu.sg/handle/10635/115922||ISSN:||15356108||DOI:||10.1016/j.ccr.2013.10.003|
|Appears in Collections:||Staff Publications|
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