XRCC1 rs1799782 Promotes DNA Damage Repair in Lung Cancer Cells by Enhancing Its Binding to FOXA1 to Facilitate FOXA1 -Mediated Transcription of XRCC1

( ) rs1799782 polymorphism is associated with an increased risk of lung cancer (LC). The aim of this study is to analyze the underlying biological mechanisms. Dual luciferase reporter assay was utilized to verify the impact of polymorphism upon promoter activity of . Cell counting kit-8 (CCK-8) assay, colony formation assay, senescence-associated beta-galactosidase (SA-β-gal) staining, and immunofluorescent staining were used to assess the viability, proliferation, senescence, and DNA damage of LC cells. Senescence-related proteins (cyclin dependent kinase inhibitor 1A (P21) and eukaryotic translation elongation factor 1-alpha (EF1A)) were quantified by Western blot. Chromatin immunoprecipitation was applied to validate the binding affinity of ( ) and . -specific short hairpin RNA (sh ) was used to perform the rescue assay. In LC cells, rs1799782 promoted viability and proliferation, inhibited senescence, and resulted in upregulation of EF1A as well as downregulation of P21 and ( ). rs1799782 promoted -mediated transcription of through enhancing its binding to . sh counteracted the effects of rs1799782 upon the viability, proliferation, and senescence of LC cells. rs1799782 promotes DNA damage repair in LC cells through enhancing its binding to , which facilitates -mediated transcription of .