Lung adenocarcinoma is one of the malignant tumors in the world. This study aimed to explore the biological mechanism of GINS2 in lung adenocarcinoma. 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. 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. 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. © 2020 Tian et al.