miR-532抑制Sema4C逆转宫颈癌细胞上皮间质转化及增加对顺铂化疗的敏感性

目的:探讨miR-532抑制Sema4C逆转宫颈癌细胞上皮间质转化及增加对顺铂化疗敏感性的作用。方法:检测宫颈癌细胞Caski经过沉默Sema4C表达后EMT标志物表达水平；利用Transwell迁移与侵袭实验检测沉默Sema4C表达所引起的宫颈癌细胞Caski迁移与侵袭能力变化；预测Sema4C是miR-532直接的靶基因并用双荧光素酶实验检测荧光素酶活性；Western blotting及qRT-PCR检测表达miR-532后EMT标志物E-cadherin、Vimentin、Snail的蛋白表达水平及mRNA表达水平；利用Transwell迁移与侵袭实验检测Caski细胞经过转染miR-532 mimic后迁移、侵袭能力的变化；CCK8检测过表达 miR-532及沉默 Sema4C对宫颈癌细胞顺铂化疗敏感性的影响。结果:Sema4C参与调节宫颈癌细胞Caski上皮间质转化，下调Sema4C可逆转这一过程；Sema4C是miR-532直接的靶基因；miR-532可逆转宫颈癌细胞的EMT；过表达miR-532及沉默Sema4C能显著提高宫颈癌细胞对顺铂敏感性。结论:miR-532通过抑制靶基因Sema4C的表达水平在宫颈癌中扮演抑癌基因的角色，逆转了宫颈癌细胞Caski的上皮间质转化及增加对顺铂化疗的敏感性。

miR-532 inhibits Sema4C to reverse epithelial-mesenchymal transition of cervical cancer cells and increase the sensitivity to cisplatin chemotherapy

Objective:To explore the role of miR-532 inhibits Sema4C to reverse epithelial-mesenchymal transition(EMT) of cervical cancer cells and increase the sensitivity to cisplatin chemotherapy.Methods:The expression level of EMT markers in Caski was detected after silencing Sema4C expression in cervical cancer cells.Transwell migration and invasion assay were used to detect Caski migration and invasion ability of cervical cancer cells induced by silencing Sema4C expression.It was predicted that Sema4C was the direct target gene of miR-532 and the luciferase activity was detected by double luciferase assay.The expression of miR-532 by Western blotting and qRT-PCR could lead to the protein expression levels and mRNA expression levels of E-cadherin，Vimentin and Snail，EMT markers.Transwell migration and invasion assay were used to detect the changes of migration and invasion ability of Caski cells after transfection with miR-532 mimic.CCK8 detected the sensitivity of overexpressed miR-532 and silenced Sema4C to cisplatin chemotherapy in cervical cancer cells.Results:Sema4C was involved in regulating Caski epithelial-mesenchymal transition of cervical cancer cells，and down-regulation of Sema4C could reverse this process.Sema4C is the direct target gene of miR-532.miR-532 can reverse EMT of cervical cancer cells.Overexpression of miR-532 and silencing of Sema4C significantly increased the sensitivity of cervical cancer cells to cisplatin.Conclusion:This study revealed that miR-532 plays the role of tumor suppressor gene in cervical cancer by inhibiting the expression level of target gene Sema4C，reversing the epithelial-mesenchymal transition of Caski cells in cervical cancer and increasing the sensitivity to cisplatin chemotherapy，indicating that miR-532 has the potential to become a new target for the diagnosis and treatment of cervical cancer.