ArticleOncoTargets and therapy2025
Targeting ANXA4 to Overcome Cisplatin Resistance in Ovarian Cancer: A Bioinformatics and in Vitro Study.
Article in OncoTargets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Molecular Insights from Differential Proteomic Profiling of Premalignant Cervical Lesions and Cervical Cancer.Pathogens (Basel, Switzerland) · 2026Article
- Integrated Analyses IdentifyInternational journal of molecular sciences · 2026Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ovarian cancer is a leading cause of gynecologic cancer-related deaths, with cisplatin (DDP) resistance posing a significant challenge to effective treatment. Understanding the molecular mechanisms underlying DDP resistance is crucial for developing new therapeutic strategies.This study aimed to explore the molecular mechanisms of DDP resistance in ovarian cancer, focusing on identifying key genes involved in this process. Methods: Differential gene expression analysis was conducted using three GEO datasets to identify genes associated with DDP resistance in ovarian cancer cells. Functional enrichment analysis was performed to elucidate the biological pathways involved. ANXA4 was identified as a key gene, and its role was further investigated through in vitro experiments, including gene silencing and overexpression assays, to assess its impact on cell viability, apoptosis, and epithelial-mesenchymal transition (EMT) markers. Results: A total of 33 common differentially expressed genes (DEGs) were identified, with ANXA4 significantly upregulated in DDP-resistant ovarian cancer cells. Functional analysis revealed that these DEGs, including ANXA4, were involved in pathways related to cell survival, proliferation, and apoptosis. In vitro experiments showed that silencing ANXA4 decreased cell viability, increased apoptosis, and reversed EMT markers in DDP-resistant cells. Conversely, ANXA4 overexpression enhanced resistance to DDP, as evidenced by increased cell viability, reduced apoptosis, and upregulation of EMT markers. Conclusion: ANXA4 plays a critical role in promoting DDP resistance in ovarian cancer by enhancing cell survival, inhibiting apoptosis, and maintaining EMT characteristics. Targeting ANXA4 may offer a novel therapeutic strategy to overcome chemoresistance and improve treatment outcomes in patients with ovarian cancer. Future studies should validate these findings in vivo and explore the precise molecular mechanisms by which ANXA4 modulates DDP resistance.
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