Shi Fengjuan, Wei Yumei, Huang Yingmei, Yao Desheng
Department of Gynecologic Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, People's Republic of China.
Department of Gynecology, the Fifth Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, People's Republic of China.
Cancer Manag Res. 2025 Jan 24;17:131-143. doi: 10.2147/CMAR.S496925. eCollection 2025.
Cervical cancer is the fourth leading cause of cancer-related death in women. Furthermore, owing to its significant risk of recurrence or metastasis, the overall prognosis of patients with cervical cancer remains poor. Activating transcription factor 5 (ATF5) plays a crucial role in cell proliferation, survival, and apoptosis, and has been implicated in the progression of various types of cancer. However, the biological function and precise mechanism of ATF5 in cervical cancer remain unclear. This study, aimed to explore the function of ATF5 and its potential mechanisms in cervical cancer.
Quantitative real-time PCR, Western blot and immunohistochemistry were used to detect the expression of ATF5 in cervical cancer tissues and cell lines. Knockdown ATF5 expression in cervical cancer cell lines was constructed using lentivirus-mediated shRNA to explore the role of ATF5 in cervical cancer through cell viability, transwell, and wound healing experiments. The expression of Wnt3a and β-catenin were investigated using quantitative real-time PCR and Western blot.
ATF5 was overexpressed in cervical cancer, and upregulation of ATF5 expression was associated with a poor prognosis. ATF5 knockdown inhibited the proliferation, migration and invasion abilities of cervical cancer cells. Furthermore, the downregulation of ATF5 led to the suppression of Wnt3a and β-catenin expression, which are key molecules in the Wnt/β-catenin signaling pathway.
ATF5 promotes tumorigenic capability in cervical cancer through the Wnt/β-catenin signaling pathway. ATF5 may be a potential prognostic biomarker and therapeutic target in the management of cervical cancer.
宫颈癌是女性癌症相关死亡的第四大原因。此外，由于其复发或转移的风险很大，宫颈癌患者的总体预后仍然很差。激活转录因子5（ATF5）在细胞增殖、存活和凋亡中起关键作用，并与多种癌症的进展有关。然而，ATF5在宫颈癌中的生物学功能和确切机制仍不清楚。本研究旨在探讨ATF5在宫颈癌中的功能及其潜在机制。
采用定量实时PCR、蛋白质印迹法和免疫组织化学法检测宫颈癌组织和细胞系中ATF5的表达。利用慢病毒介导的短发夹RNA构建宫颈癌细胞系中ATF5表达下调模型，通过细胞活力、Transwell和伤口愈合实验探讨ATF5在宫颈癌中的作用。采用定量实时PCR和蛋白质印迹法研究Wnt3a和β-连环蛋白的表达。
ATF5在宫颈癌中高表达，ATF5表达上调与预后不良相关。敲低ATF5可抑制宫颈癌细胞的增殖、迁移和侵袭能力。此外，ATF5的下调导致Wnt3a和β-连环蛋白表达受到抑制，而Wnt3a和β-连环蛋白是Wnt/β-连环蛋白信号通路中的关键分子。
ATF5通过Wnt/β-连环蛋白信号通路促进宫颈癌的致瘤能力。ATF5可能是宫颈癌管理中的一个潜在预后生物标志物和治疗靶点。
