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

Background: () rs1799782 polymorphism is associated with an increased risk of lung cancer (LC). The aim of this study is to analyze the underlying biological mechanisms.

Methods: 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.

Results: 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.

Conclusions: rs1799782 promotes DNA damage repair in LC cells through enhancing its binding to , which facilitates -mediated transcription of .