摘要
目的探索SKA1在子宫内膜癌中的表达及作用机制。方法分析GEPIA数据库资料中SKA1对EC的影响。RT-qPCR法检测SKA1在肿瘤组织及正常组织中、人子宫内膜癌细胞及正常细胞中的表达水平。通过CCK-8实验、平板细胞克隆形成实验、流式细胞术、划痕实验、Transwell法测RL95-2、Ishiwaka细胞的增殖、克隆形成、细胞的周期分布、迁移及侵袭情况。蛋白质免疫印迹法检测两组细胞中SKA1、CyclinD1、MMP2、MMP9、GAPDH、P13K、p-P13K、AKT和p-AKT水平。结果SKA1在EC中高表达,且SKA1高表达与EC患者生存率降低有关。SKA1在肿瘤组织、RL95-2和Ishiwaka细胞中呈现高表达。si-SKA1可抑制RL95-2和Ishiwaka细胞的增殖、迁移和侵袭能力。SKA1可通过抑制PI3K/AKT信号通路,下调SKA1、CyclinD1、MMP2、MMP9的表达。结论SKA1通过PI3K/AKT通路促进子宫内膜癌细胞的增殖、迁移和侵袭能力。
Objective To explore the expression and mechanism of SKA1 in endometrial cancer.Methods Analyzed the effect of SKA1 on EC in GEPIA database.RT-qPCR was used to detect the expression levels of SKA1 in tumor tissues and normal tissues,as well as in human endometrial cancer cells and normal cells.The proliferation,colony formation,cell cycle distribution,migration,and invasion of RL95-2 and Ishiwaka cells were measured by CCK-8 assay,plate cell clone formation assay,flow cytometry,scratch assay,and Transwell method.Protein immunoblotting was used to detect the levels of SKA1,CyclinD1,MMP2,MMP9,GAPDH,P13K,p-P13K,AKT and p-AKT in two groups of cells.Results SKA1 was highly expressed in EC,and its high expression was associated with reduced survival rate in EC patients.SKA1 showed high expression in tumour tissues,RL95-2 and Ishiwaka cells.Si-SKA1 could inhibit the proliferation,migration and invasion ability of RL95-2 and Ishiwaka cells.SKA1 could downregulate the expression of SKA1,CyclinD1,MMP2 and MMP9 by inhibiting the PI3K/AKT pathway.Conclusion SKA1 can promote the proliferation,migration and invasion of endometrial cancer cells through the PI3K/AKT pathway.
作者
闫亚楠
龚咪
张磊
YAN Yanan;GONG Mi;ZHANG Lei(Department of Gynecology,The Affiliated Huai’an No.1 People's Hospital of Nanjing Medical University,Huai’an 223000,Jiangsu,China)
出处
《西部医学》
2025年第9期1274-1279,共6页
Medical Journal of West China
基金
淮安市基础研究计划面上项目(HABL2023064)。
