HPV诱导的miR-21-5p通过PI3K/AKT途径促进宫颈癌细胞的上皮间质转化和肿瘤进展OA
HPV-induced miR-21-5p promotes epithelial-mesenchymal transition and tumor progression in cervical cancer cells via the PI3K/AKT pathway
目的 探讨人乳头瘤病毒(HPV)诱导的 miR-21-5p对宫颈癌细胞的上皮间质转化(EMT)和肿瘤进展的影响.方法 HPV(+)宫颈癌细胞分为 mimic-NC组、miR-21-5p-mimic组、inhibitor-NC和 miR-21-5p-inhibitor组.采用实时荧光定量聚合酶链式反应(qPCR)分析 miR-21-5p在 HPV(+)宫颈癌细胞中的表达,Transwell实验检测细胞迁移和侵袭情况,Western blot检测上皮型钙黏蛋白(E-cadherin)、神经型钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、磷酸化磷脂酰肌醇3-激酶(p-PI3K)、磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(AKT)、磷酸化蛋白激酶B(p-AKT)和β-肌动蛋白(β-actin)的表达.结果 与 HPV(-)C33A相比,HPV16(+)SiHa和 HPV18(+)HeLa中 miR-21-5p的表达显著增加(F=51.35,P<0.01).Transwell实验结果显示,与 mimic-NC组相 比,miR-21-5p-mimic组细胞迁移和侵袭数量显著提高(t=6.73,5.64,P<0.01);而与inhibitor-NC组相比,miR-21-5p-inhibitor组细胞迁移和侵袭数量显著降低(t=17.32,15.46,P<0.01).Western blot检测结果显示,与 mimic-NC组相比,miR-21-5p-mimic组细胞中E-cadherin表 达 降 低,N-cadherin和 Vimentin表达升高;而与inhibitor-NC组 相 比,miR-21-5p-inhibitor组细胞中E-cadherin表达升高,N-cadherin和 Vimentin表达降低.与 mimic-NC组 相 比,miR-21-5p-mimic组细胞中p-PI3K和p-AKT显著提高;而与inhibitor-NC组 相 比,miR-21-5p-inhibitor组细胞中p-PI3K和p-AKT显著降低.结论 HPV诱导的 miR-21-5p可能通过激活PI3K/AKT途径促进宫颈癌细胞的迁移、侵袭和上皮间质转化.
Objective To investigate the effects of HPV-induced miR-21-5p on epithelial-mesenchymal transition(EMT)and tumour progression in cervical carcinoma cells.Methods HPV(+)cervical cancer cells were divided into the mimic-NC group,miR-21-5p-mimic group,inhibitor-NC group,and miR-21-5p-inhibitor group.Real-time fluorescence quantitative polymerase chain reaction(qPCR)was used to analyze the expression of miR-21-5p in HPV(+)cervical cancer cells,and Transwell assay was detected cell migration and invasion.The expression of E-cadherin,N-cadherin,Vimentin,phosphorylated phosphatidylinositol 3-kinase(p-PI3K),phosphatidylinositol 3-kinase(PI3K),protein kinase B(AKT),phosphorylated protein kinase B(p-AKT)proteins and β-actin were detected by Western blot.Results Compared with HPV(-)C33A cells,the expression of miR-21-5p was significantly increased in HPV16(+)SiHa and HPV18(+)HeLa cells(F=51.35,P<0.01).Transwell assay results demonstrated that,compared with the mimic-NC group,the miR-21-5p-mimic group exhibited significantly increased cell migration and invasion(t=6.73 and 5.64,respectively P<0.01);whereas compared with the inhibitor-NC group,cell migration and invasion were markedly reduced in the miR-21-5p-inhibitor group(t=17.32 and 15.46,respectively P<0.01).Western blot analysis revealed that,compared with the mimic-NC group,miR-21-5p-mimic-treated cells exhibited reduced E-cadherin expression alongside increased N-cadherin and Vimentin expression.Conversely,compared with the inhibitor-NC group,miR-21-5p-inhibitor group cells demonstrated elevated E-cadherin expression alongside decreased N-cadherin and vimentin expression.Compared with the mimic-NC group,p-PI3K and p-AKT levels were significantly elevated in miR-21-5p-mimic group cells.Conversely,compared with the inhibitor-NC group,p-PI3K and p-AKT levels were markedly reduced in miR-21-5p-inhibitor group cells.Conclusion HPV-induced miR-21-5p may promote migration,invasion and epithelial-mesenchymal transition in cervical cancer cells by activating the PI3K/AKT pathway.
徐丽娜;崔梦瑶;袁向珍
内蒙古医科大学附属医院健康管理中心,内蒙古 呼和浩特 010010内蒙古医科大学附属医院健康管理中心,内蒙古 呼和浩特 010010内蒙古医科大学附属医院健康管理中心,内蒙古 呼和浩特 010010
医药卫生
HPVmiR-21-5pPI3K/AKT途径宫颈癌上皮间质转化
HPVmiR-21-5pPI3K/AKT pathwaycervical cancerepithelial-mesenchymal transition
《中国妇幼健康研究》 2026 (5)
64-69,6
内蒙古医科大学青年创新基金项目(YKD2018QNCX072)
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