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Targeting ANXA4 to Overcome Cisplatin Resistance in Ovarian Cancer: A Bioinformatics and in Vitro Study
1Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, 430060, People's Republic of China.
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.
Insights
This study reveals Annexin A4 (ANXA4) promotes cisplatin resistance in ovarian cancer by boosting cell survival and maintaining cancer cell traits. Targeting ANXA4 may overcome chemoresistance and improve patient outcomes.
Area of Science:
- Gynecologic Oncology
- Cancer Genomics
- Molecular Mechanisms of Cancer
Background:
- Ovarian cancer is a leading cause of cancer deaths, with cisplatin resistance a major treatment obstacle.
- Understanding molecular drivers of cisplatin resistance is vital for developing new ovarian cancer therapies.
Purpose of the Study:
- To investigate the molecular mechanisms of cisplatin resistance in ovarian cancer.
- To identify key genes contributing to cisplatin resistance in ovarian cancer cells.
Main Methods:
- Differential gene expression analysis of three GEO datasets identified 33 common differentially expressed genes.
- Functional enrichment analysis pinpointed pathways involved in cell survival and apoptosis.
- In vitro experiments assessed the role of ANXA4 via gene silencing and overexpression.
Main Results:
- ANXA4 was significantly upregulated in cisplatin-resistant ovarian cancer cells.
- Silencing ANXA4 reduced cell viability, increased apoptosis, and reversed EMT markers.
- Overexpressing ANXA4 enhanced cisplatin resistance, increased cell viability, and upregulated EMT markers.
Conclusions:
- ANXA4 promotes cisplatin resistance in ovarian cancer by enhancing cell survival, inhibiting apoptosis, and maintaining epithelial-mesenchymal transition (EMT).
- Targeting ANXA4 presents a potential therapeutic strategy to overcome chemoresistance in ovarian cancer.
- Further in vivo studies are needed to validate ANXA4's role and elucidate its precise mechanisms in modulating cisplatin resistance.
