Background: Lung adenocarcinoma is one of the malignant tumors in the world. This study aimed to explore the biological mechanism of GINS2  in lung adenocarcinoma.
Materials and Methods: Raw data were downloaded from GEO. WGCNA co-expression network and PPI network were established to identify the hub gene. The expression profile and clinical features of GINS2  were collected from TCGA-LUAD cohort. Survival analysis in TCGA-LUAD cohort was plotted by R package. GSEA was analyzed via GSEA software. MTS, Transwell and apoptosis assays were used to detect the proliferation, migration and apoptotic abilities of lung adenocarcinoma cells.
Results: GINS2  was identified as the hub gene via WGCNA co-expression network and PPI network. Higher GINS2  expressions were observed in TCGA-LUAD cohort, GSE32863 and clinical samples dataset. Overexpression of GINS2  had a significantly negative connection with poor survival outcome. GSEA results revealed that GINS2  could be enriched in “HALLMARK_G2M_CHECKPOINT”, “HALLMARK_E2F_TARGETS”, “HALLMARK_DNA_REPAIR” and “HALLMARK_MYC_TARGETS_V2”. Overexpression of GINS2  promoted tumor cell proliferation and migration and suppressed cell apoptosis.
Conclusion: Our results explored that GINS2  functioned as an oncogene in lung adenocarcinoma, and suggested that GINS2  could act as a promising prognosis biomarker for lung adenocarcinoma.
Keywords: GINS2 , lung adenocarcinoma, WGCNA, biological function