Genome-wide gene expression analysis of EGFR inhibitor erlotinib-resistant and -sensitive head and neck squamous cell carcinoma cell lines Cal-27, SCC-25, FaDu, and SQ20B

Despite the role of epidermal growth factor receptor (EGFR) signaling in head and neck squamous cell carcinoma (HNSCC) development and progression, clinical trials involving EGFR tyrosine kinase inhibitors (TKIs) have yielded poor results in HNSCC patients. Mechanisms of acquired resistance to the EGFR TKI erlotinib was investigated by developing erlotinib-resistant HNSCC cell lines (Cal-27, SCC-25, FaDu, and SQ20B) and comparing their gene expression profiles with their parental erlotinib-sensitive HNSCC cell lines using microarray analyses. Subsequent pathway and network analyses displayed a significant upregulation in immune response pathways. Role of immune/inflammatory signaling in acquired resistance to erlotinib in HNSCC was investigated. Total RNA was isolated from erlotinib-resistant and erlotinib-sensitive head and neck squamous cell carcinoma cell lines Cal-27, SCC-25, FaDu, and SQ20B subjected to 48 hours of 0.01% DMSO (i.e., vehicle control).