Found programs:
Authors:Li Xuan; Cheng Hao; Fang Yue
Keywords:autophagy;programmed death ligand 1;EGFR-TKI resistance;non small cell lung carcinoma
DOI:10.19405/j.cnki.issn1000-1492.2021.10.006
〔Abstract〕 Objective To investigate the effect of autophagy on drug sensitivity of PC9/GR and programmed death ligand-1(PD-L1) in gefitinib-resistant lung adenocarcinoma cellsin vitro. Methods Real-time fluorescence quantitative PCR and Western blot assay were performed to detect the expression levels of autophagy-related proteins LC3 II/LC3 I, Beclin1 and PD-L1 in gefitinib-sensitive cell line PC9 and gefitinib-resistant cell line PC9/GR; CCK-8 assay was performed to detect the sensitivity of PC9 and PC9/GR cells to gefitinib and the inhibition of PC9/GR; The expression of LC3 II/LC3 I, p62 and PD-L1 in PC9/GR cells after autophagy was detected by Western blot. Results The expression of autophagy and PD-L1 was higher in PC9/GR cells than that in PC9 cells, and CCK-8 assay showed that the IC50 for gefitinib was higher in PC9/GR cells than that in PC9 cells, and the sensitivity of PC9/GR cells to gefitinib was partially restored after inhibition of autophagy(P<0.05). PD-L1 expression increased and inhibited autophagy PD-L1 expression decreased with the time and concentration of autophagy inhibitor treatment(P<0.05). Conclusion The results ofin vitroexperiments suggest that inhibition of autophagy may enhance the sensitivity of lung adenocarcinoma resistant cells to gefitinib, suggesting that PD-L1 may be regulated by autophagy and that PD-L1 may be involved in the reversal of gefitinib resistance by inhibition of autophagyin vitro.