Liang Guanying, Qi Zijuan, Du Chun
Department of Pathology, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Harbin, Heilongjiang, 150081, China.
Department of Pathology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang, 150000, China.
Open Life Sci. 2024 Dec 31;19(1):20220990. doi: 10.1515/biol-2022-0990. eCollection 2024.
To investigate the biological role of MFAP5 in endometrial cancer (EC). HEC-1-A and Ishikawa cells overexpressing MFAP5 were created. Cell proliferation, apoptosis, migration, and invasion were evaluated using CCK8, colony formation, flow cytometry, and transwell assays. A western blot was used to analyze the expression of markers affiliated with the epithelial-mesenchymal transition process and AKT/mTOR pathway. As a result, MFAP5 was found to be down-regulated in EC. Overexpression of MFAP5 suppressed proliferation and promoted apoptosis of HEC-1-A and Ishikawa cells, as evidenced by the inhibition of cell viability and colony formation, and the increase in cell apoptosis rate. Besides, overexpression of MFAP5 attenuated the abilities of cell migration and invasion, as well as reduced MMP2 and MMP9 protein expression. Furthermore, E-cadherin protein level was elevated, while N-cadherin and α-SMA protein levels were decreased, and the phosphorylation of AKT and mTOR was reduced in cells overexpressing MFAP5. Our findings indicate that MFAP5 overexpression inhibits the malignant behaviors of EC cells, possibly by blocking the AKT/mTOR pathway, suggesting that MFAP5 may be a new therapeutic target for EC.
为研究MFAP5在子宫内膜癌（EC）中的生物学作用。构建了过表达MFAP5的HEC-1-A和Ishikawa细胞。使用CCK8、集落形成、流式细胞术和Transwell实验评估细胞增殖、凋亡、迁移和侵袭。采用蛋白质免疫印迹法分析与上皮-间质转化过程及AKT/mTOR信号通路相关标志物的表达。结果发现，MFAP5在EC中表达下调。MFAP5过表达抑制了HEC-1-A和Ishikawa细胞的增殖并促进其凋亡，这通过细胞活力和集落形成的抑制以及细胞凋亡率的增加得以证明。此外，MFAP5过表达减弱了细胞迁移和侵袭能力，并降低了MMP2和MMP9蛋白表达。此外，在过表达MFAP5的细胞中，E-钙黏蛋白水平升高，而N-钙黏蛋白和α-SMA蛋白水平降低，AKT和mTOR的磷酸化水平降低。我们的研究结果表明，MFAP5过表达可能通过阻断AKT/mTOR信号通路抑制EC细胞的恶性行为，提示MFAP5可能是EC的一个新的治疗靶点。
