AurkC regulates the expression of DNA damage repair proteins and affects the acquired resistance to gefitinib in non-small cell lung cancer

AimTo study the mechanism of AurkC resistance to gefitinib in non-small cell lung cancer cells.MethodsHuman lung cancer HCC827 and gefitinib resistant HCC827GR cells were cultured in vitro, cell proliferation was detected by MTT assay, and AurkC protein expression was detected in the drug-resistant cell model. AurkC overexpression cell line was constructed, and the protein expression level of γ-H2AX (S139) in the nucleus and DNA damage foci in nucleus were detected by Western blot and immunofluorescence staining. The degree of DNA damage was assessed by comet assay, and the expression of proteins related to DNA damage repair was detected by Western blot.ResultsThe IC50 of HCC827 and the IC50 of HCC827GR were 0.004±0.001 μmol·L-1 and the IC50 of HCC827GR was 14.630±5.348 μmol·L-1 and the drug resistance index was 3 402.326, indicating that HCC827GR was highly tolerant to gefitinib. Western blot results showed that the expression level of AurkC in drug-resistant cell lines was much higher (P P P P P ConclusionAurkC promotes gefitinib resistance in non-small cell lung cancer by inhibiting the expression of DNA damage repair related proteins.