Abstract 5238: Lung adenocarcinoma harboring EGFR L858R mutation has increased invasive ability through up-regulation of CXCR4

Abstract

Abstract Our previous study disclosed EGFR L858R mutation rate of lung adenocarcinoma with malignant pleural effusions of is higher than that of surgically resected lung adenocarcinoma (Wu et al, Eur Respir J 2008). The molecular mechanism is not clear. The chemokine receptor CXCR4 has recently been shown to mediate the movement of malignant cancer cells to specific organs. Stable clones of wild type and mutant L858R EGFR from lung cancer cell line H1299 were obtained from Dr. Chen (Chen YR et al Oncogene 2006). The Invasive ability of L858R EGFR H1299 cells was higher than that of wild type EGFR H1299 cell. L858R EGFR H1299 cell had higher CXCR4 expression, which was required for L858R EGFR-mediated invasion in vitro. Up-regulation of CXCR4 in L858R EGFR H1299 cell promoted invasion via increased activity of ERK. These results provide a plausible mechanism for L855R EGFR-mediated lung tumor metastasis and establish a functional link between mutant EGFR and CXCR4 signaling pathways. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5238. doi:10.1158/1538-7445.AM2011-5238