Please use this identifier to cite or link to this item:
https://doi.org/10.1016/j.ccr.2013.10.003
DC Field | Value | |
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dc.title | Runx3 Inactivation Is a Crucial Early Event in the Development of Lung Adenocarcinoma | |
dc.contributor.author | Lee, Y.-S. | |
dc.contributor.author | Lee, J.-W. | |
dc.contributor.author | Jang, J.-W. | |
dc.contributor.author | Chi, X.-Z. | |
dc.contributor.author | Kim, J.-H. | |
dc.contributor.author | Li, Y.-H. | |
dc.contributor.author | Kim, M.-K. | |
dc.contributor.author | Kim, D.-M. | |
dc.contributor.author | Choi, B.-S. | |
dc.contributor.author | Kim, E.-G. | |
dc.contributor.author | Chung, J.-H. | |
dc.contributor.author | Lee, O.-J. | |
dc.contributor.author | Lee, Y.-M. | |
dc.contributor.author | Suh, J.-W. | |
dc.contributor.author | Chuang, L. | |
dc.contributor.author | Ito, Y. | |
dc.contributor.author | Bae, S.-C. | |
dc.date.accessioned | 2014-12-12T07:34:10Z | |
dc.date.available | 2014-12-12T07:34:10Z | |
dc.date.issued | 2013-11-11 | |
dc.identifier.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 | |
dc.identifier.issn | 15356108 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/115922 | |
dc.description.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. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.ccr.2013.10.003 | |
dc.source | Scopus | |
dc.type | Article | |
dc.contributor.department | CANCER SCIENCE INSTITUTE OF SINGAPORE | |
dc.description.doi | 10.1016/j.ccr.2013.10.003 | |
dc.description.sourcetitle | Cancer Cell | |
dc.description.volume | 24 | |
dc.description.issue | 5 | |
dc.description.page | 603-616 | |
dc.description.coden | CCAEC | |
dc.identifier.isiut | 000327005100008 | |
Appears in Collections: | Staff Publications |
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