Abstract: Objective To explore the potential role of programmed cell death ligand 1 ( PD-L1) in icotinib resistance by using epidermal growth factor receptor (EGFR) -mutant non-small cell lung cancer (NSCLC) cells. Methods The expression levels of p-EGFR and PD-L1 in A549, HCC827 and PC-9 cells were detected by real-time fluorescent quantitative PCR ( qRT-PCR) and Western blotting. MTT method was used to evaluate the sensitivity of HCC827 and PC-9 cells to icotinib. PD-L1 knockout cells were used to evaluate the effect of PD-L1 on the sensitivity of EGFR-mutant NSCLC cells to icotinib, and the patient-derived tumor xenografts mouse model was used for the in vivo experiments. Results Compared with the A549 cells, the expression levels of p-EGFR and PD-L1 were higher in the HCC827 and PC-9 cells. Icotinib significantly inhibited the proliferation and enhanced the apoptosis of HCC827 and PC-9 cells. Knockout of PD-L1 significantly reduced the inhibition of icotinib on HCC827 and PC-9 cells. Compared with the sh-NC + icotinib group, PD-L1 knockout reduced the sensitivity of EGFR-mutant NSCLC cells to icotinib in vivo. Conclusion Icotinib could inhibit EGFR-mutant NSCLC cells, and PD-L1 contribute to the icotinib sensitivity in EGFR-mutant NSCLC cells. 

Key words: non-small cell lung cancer, epidermal growth factor receptor, icotinib, PD-L1