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ORIGINAL RESEARCH article

Front. Mol. Biosci.

Sec. Molecular Diagnostics and Therapeutics

Volume 12 - 2025 | doi: 10.3389/fmolb.2025.1661558

This article is part of the Research TopicClinical Molecular Biological Characteristics of Malignant TumorsView all 4 articles

Integrated Analysis and Experimental Validation of E2F2 as a Potential 1 Prognostic Biomarker and Its Oncogenic Roles in Serous Ovarian Cancer 2

Provisionally accepted
  • 1Fudan University, Shanghai, China
  • 2Fifth People's Hospital of Shanghai Fudan University, Shanghai, China

The final, formatted version of the article will be published soon.

Background. This study evaluated E2F2’s prognostic role in serous ovarian cancers (SOCs) and explored its biological functions, immune cell infiltration links, and therapeutic implications. Methods. Integrating TCGA/GTEx data, we used bioinformatics tools (ssGSEA, Immunophenoscore, 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, HASPIN) showed strong co-expression. Pathway analysis of 808 differentially expressed genes linked E2F2 to immune cell recruitment, including CD4+ T cells, NK cells, and Tregs; low E2F2 levels 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. Conclusions. High E2F2 expression marks poor prognosis and immune cell infiltration in SOCs, acting 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.

Keywords: Serous Ovarian Cancer(SOC), E2F transcription factor 2 (E2F2), tumor microenvironment(TME), chemotherapy resistance, cell cycle regulator

Received: 08 Jul 2025; Accepted: 21 Aug 2025.

Copyright: © 2025 Jiang, Fei, Yang, Chen and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Fengyin Jiang, Fudan University, Shanghai, China
Liwen Zhang, Fifth People's Hospital of Shanghai Fudan University, Shanghai, China

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