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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Cancer Discov. 2013 Sep 27;3(12):10.1158/2159-8290.CD-13-0310. doi: 10.1158/2159-8290.CD-13-0310

Figure 4. EGFR pathway activation in human bronchial epithelial cells induces PD-L1 expression.

Figure 4

(a) Microarray expression profiling analysis of established cell lines from human NSCLC patients. Black and red bars indicate identified Kras or EGFR mutations respectively. TGF-alpha, met proto-oncogene (MET), heparin-binding EGF-like growth factor (HBEGF), EREG and BTC are EGFR ligands. (b) PD-L1 up-regulation in BEAS-2B bronchial epithelial cell lines transduced with vectors encoding Kras mutation (G12V) or EGFR mutation (T790M-Del19), as assessed by qPCR and flow cytometry (c-e). Reduction of PD-L1 expression in NSCLC cell lines 72 hours after EGFR TKI treatment at the indicated concentrations (in the absence of drug-induced apoptosis) (c) EGFR-del19 mutant PC-9 and HCC827 NSCLCs (d), Gefitinib resistant H1975 NSCLC (e) EGFR wild type Kras mutant H358 NSCLC. Representative results from 3 independent experiments are shown. (f) Sections of formalin fixed patient tumors carrying EGFR mutations stained with H&E or PD-L1. Top panel, high expression on tumor cell membrane; middle panel, low expression on membrane; bottom panel, expression on macrophages. Scale bars show 100 μm.