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已发表论文
靶向 ANXA4 克服卵巢癌顺铂耐药性：一项生物信息学和体外研究
Received 9 July 2025
Accepted for publication 10 October 2025
Published 7 November 2025 Volume 2025:18 Pages 1243—1256
DOI https://doi.org/10.2147/OTT.S552516
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr John Riches
Yong Wang,1 Qingzhen Xie2
1Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China; 2Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China
Correspondence: Qingzhen Xie, Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China, Email 13387554568@163.com
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.
Keywords: ovarian cancer, cisplatin resistance, ANXA4, cell viability, apoptosis, epithelial-mesenchymal transition
1Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China; 2Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China
Correspondence: Qingzhen Xie, Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China, Email 13387554568@163.com
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.
Keywords: ovarian cancer, cisplatin resistance, ANXA4, cell viability, apoptosis, epithelial-mesenchymal transition