CPEB1通过抑制上皮间质转化逆转卵巢癌细胞化疗耐药的研究

doi:10.19586/j.2095-2341.2025.0124

生物技术进展 ›› 2026, Vol. 16 ›› Issue (1): 205-212.DOI: 10.19586/j.2095-2341.2025.0124

• 研究论文 • 上一篇

CPEB1通过抑制上皮间质转化逆转卵巢癌细胞化疗耐药的研究

郭利佩, 张群昌, 曹馨, 张秀玲()

西电集团医院妇产科，西安 710077

收稿日期:2025-09-17 接受日期:2025-11-12 出版日期:2026-01-25 发布日期:2026-02-12
通讯作者: 张秀玲
作者简介:第一联系人：郭丽佩 E-mail: 2223562864@qq.com；
基金资助:
西安市卫生健康委员会科研项目(2021yb51)

Research on CPEB1 Reversing Chemoresistance of Ovarian Cancer Cells by Inhibiting Epithelial-mesenchymal Transition

Lipei GUO, Qunchang ZHANG, Xin CAO, Xiuling ZHANG()

Department of Gynaecology and Obstetrics，Xidian Group Hospital，Xi'an 710077，China

Received:2025-09-17 Accepted:2025-11-12 Online:2026-01-25 Published:2026-02-12
Contact: Xiuling ZHANG

摘要/Abstract

摘要：

研究旨在探讨胞质多聚腺苷酸化结合蛋白1（cytoplasmic polyadenylation element-binding 1，CPEB1）在卵巢癌顺铂（cis-diamminedichloroplatinum Ⅱ, DDP）耐药性中的作用及其相关机制。通过基因表达谱交互式分析平台（gene expression profiling interactive analysis, GEPIA）和基因表达数据库（gene expression omnibus, GEO）分析CPEB1在卵巢癌组织及耐药细胞系中的表达；采用浓度梯度递增法构建卵巢癌顺铂耐药细胞系A2780/DDP和SKVO3/DDP，通过CCK-8法检测细胞活力及最大半数抑制浓度（half-maximal inhibitory concentration，IC??）；通过RT-qPCR和Western blot检测CPEB1 mRNA和蛋白表达。在耐药细胞A2780/DDP和SKVO3/DDP中转染CPEB1过表达质粒，通过Transwell和划痕试验检测细胞侵袭和迁移能力；通过Western blot检测上皮间质转化（epithelial-mesenchymal transition, EMT）相关标志蛋白（E-cadherin、N-cadherin、Vimentin）的表达。结果发现，CPEB1在卵巢癌组织及顺铂耐药细胞系中低表达；过表达CPEB1可显著提高耐药细胞A2780/DDP和SKVO3/DDP对顺铂的敏感性，降低其IC??值，并抑制细胞的侵袭和迁移能力。同时，过表达CPEB1可上调上皮标志物E-cadherin的表达，下调间质标志物N-cadherin和Vimentin的表达，逆转EMT进程。结果表明，CPEB1可通过抑制EMT过程增强卵巢癌细胞对顺铂的敏感性，逆转其耐药表型，有望成为卵巢癌耐药治疗的潜在靶点。

关键词: CPEB1, 卵巢癌, 顺铂, 化疗耐药, 上皮间质转化

Abstract:

This study aimed to investigate the role of cytoplasmic polyadenylation element-binding protein 1 （CPEB1） in cisplatin （cis-diamminedichloroplatinum Ⅱ， DDP） resistance in ovarian cancer and its underlying mechanism. The expression of CPEB1 in ovarian cancer tissues and drug-resistant cell lines was analyzed using the Gene Expression Profiling Interactive Analysis （GEPIA） and Gene Expression Omnibus （GEO） databases. Cisplatin-resistant ovarian cancer cell lines A2780/DDP and SKOV3/DDP were established by the concentration gradient increment method. Cell viability and half-maximal inhibitory concentration （IC??） were detected via the CCK-8 assay. The mRNA and protein expressions of CPEB1 were determined using RT-qPCR and Western blot analysis， respectively. CPEB1-overexpressing plasmids were transfected into A2780/DDP and SKOV3/DDP cells. Cell invasion and migration abilities were evaluated by Transwell assay and wound healing assay， respectively. The expressions of epithelial-mesenchymal transition （EMT）-related marker proteins （E-cadherin， N-cadherin， Vimentin） were detected by Western blot analysis. The results showed that CPEB1 was lowly expressed in ovarian cancer tissues and cisplatin-resistant cell lines. Overexpression of CPEB1 significantly enhanced the sensitivity of A2780/DDP and SKOV3/DDP cells to cisplatin， reduced their IC?? values， and inhibited cell invasion and migration capacities. Meanwhile， overexpression of CPEB1 upregulated the expression of the epithelial marker E-cadherin， downregulated the expressions of the mesenchymal markers N-cadherin and Vimentin， and thereby reversed the EMT process. In conclusion， CPEB1 can enhance the sensitivity of ovarian cancer cells to cisplatin and reverse their drug-resistant phenotype by inhibiting the EMT process， indicating that it may serve as a potential therapeutic target for overcoming cisplatin resistance in ovarian cancer.

Key words: CPEB1, ovarian cancer, cisplatin, chemotherapy resistance, epithelial-mesenchymal transition

中图分类号:

Q279

郭利佩, 张群昌, 曹馨, 张秀玲. CPEB1通过抑制上皮间质转化逆转卵巢癌细胞化疗耐药的研究[J]. 生物技术进展, 2026, 16(1): 205-212.

Lipei GUO, Qunchang ZHANG, Xin CAO, Xiuling ZHANG. Research on CPEB1 Reversing Chemoresistance of Ovarian Cancer Cells by Inhibiting Epithelial-mesenchymal Transition[J]. Current Biotechnology, 2026, 16(1): 205-212.

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CPEB1通过抑制上皮间质转化逆转卵巢癌细胞化疗耐药的研究

Research on CPEB1 Reversing Chemoresistance of Ovarian Cancer Cells by Inhibiting Epithelial-mesenchymal Transition

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