Dual blockade of EGFR and c-Met abrogates redundant signaling and proliferation in head and neck carcinoma cells.

ABSTRACT:

Purpose

Head and neck squamous cell carcinoma (HNSCC) is usually fatal, and innovative approaches targeting growth pathways are necessary to effectively treat this disease. Both the epidermal growth factor receptor (EGFR) and the hepatocyte growth factor (HGF)/c-Met pathways are overexpressed in HNSCC and initiate similar downstream signaling pathways. c-Met may act in consort with EGFR and/or be activated as a compensatory pathway in the presence of EGFR blockade.

Experimental design

Expression levels of EGFR and c-Met were determined by Western analysis in HNSCC cell lines and correlated with antitumor responses to inhibitors of these pathways.

Results

Combining the c-Met inhibitor PF2341066 with the EGFR inhibitor gefitinib abrogated HNSCC cell proliferation, invas

SUBMITTER: Xu H 

PROVIDER: S-EPMC3138116 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature