Abstract
BACKGROUND: This study evaluated the prognostic role of E2F transcription factor 2 (E2F2) in serous ovarian cancers (SOCs) and explored its biological functions, immune cell infiltration links, and therapeutic implications. METHODS: Integrating TCGA/Genotype-Tissue Expression (GTEx) data, we used bioinformatics tools (ssGSEA, Immunophenoscore, and oncoPredict) to analyze pathways and treatment responses. Validation involved RT-qPCR, Western blot analysis, cytotoxicity, and transwell assays. RESULTS: E2F2 was upregulated in SOC tumors, correlating with poorer overall/disease-free survival and higher tumor grade. Five cell-cycle-related genes (ORC1, RAD54L, CCNF, NCAPH, and HASPIN) showed strong co-expression. A pathway analysis of 808 differentially expressed genes linked E2F2 to immune cell recruitment, including CD4(+) T cells, NK cells, and Tregs; low E2F2 levels were associated with higher immune scores. High E2F2 predicted sensitivity to chemotherapy/targeted therapy, while low E2F2 correlated with anti-CTLA4 responsiveness. In vitro, E2F2 promoted metastasis. CONCLUSION: High E2F2 expression marks poor prognosis and immune cell infiltration in SOCs and thus acts as an independent risk factor. It may serve as a potential biomarker for diagnosis, patient stratification, and guiding personalized therapy. Further research could enhance SOC management.