Abstract 263: p38 MAPK is required for EGFR nuclear translocation

Abstract

Abstract The epidermal growth factor receptor (EGFR) severs as a mediator of signal cascades on the cell surface and translocates to the nucleus to control many cellular process including transcriptional regulation and DNA repair. However, the molecular mechanisms of EGFR nuclear translocation remain elusive. In this study, we show that, in addition of EGF, nuclear translocation of EGFR was induced by several p38 MAPK activating reagents including UV and cisplatin. The p38 MAPK activation correlated with EGFR nuclear translocation. To further examine the role of p38 MAPK in the EGFR nuclear translocation, p38 MAPK inhibitors, dominate negative p38 MAPK and p38 MAPK siRNA were used to inhibit UV-induced EGFR nuclear translocation. Consequently, EGFR nuclear translocation can be induced by p38 MAPK activator. Thus, we demonstrate here that p38 MAPK is required for EGFR nuclear translocation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 263.