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目的:探讨hsa-miR-214-3p对宫颈癌SiHa细胞生物学行为的影响以及可能的作用机制。方法:将hsamiR-214-3p mimics/inhibitor转染SiHa细胞,分析过表达和下调内源性hsa-miR-214-3p的表达对SiHa细胞增殖、迁移、凋亡的影响。用TargetScanHuman7.1、Pictar、miRanda、miRTarBase以及DAVID数据库进行靶基因预测和富集通路分析。结果:hsa-miR-214-3p在宫颈癌细胞中呈高表达;过表达hsa-miR-214-3p后,细胞的增殖和克隆形成能力明显增强(P<0.05);而当抑制内源性hsa-miR-214-3p的表达后,细胞的增殖能力则明显减弱(P<0.001),流式细胞仪检测细胞凋亡结果显示SiHa细胞的凋亡比例明显上升(P<0.05),Western Blot的结果显示Bcl2蛋白的表达显著下降(P<0.05);过表达hsa-miR-214-3p和抑制内源性hsa-miR-214-3p表达对SiHa细胞的迁移均没有显著的影响(P>0.05);生物信息学分析结果显示,hsa-miR-214-3p的靶基因主要富集在磷脂酰肌醇信号系统以及Wnt信号通路等。结论:过表达hsa-miR-214-3p可以促进宫颈癌细胞的增殖;抑制内源性hsa-miR-214-3p的表达可以抑制SiHa细胞的增殖并促进细胞凋亡;hsa-miR-214-3p可能通过调节Bcl2基因的表达来调控SiHa细胞的凋亡进程。上述结果为宫颈癌分子机制的研究提供了新线索,同时也为宫颈癌的临床诊断与治疗提供潜在靶点。
Objective: To investigate the effect of hsa-miR-214-3p on the biological behavior of cervical cancer SiHa cells and its possible mechanism. Methods: SiHa cells were transfected with hsamiR-214-3p mimics / inhibitor. The effects of over-expression and down-regulation of endogenous hsa-miR-214-3p on proliferation, migration and apoptosis of SiHa cells were analyzed. TargetScanHuman7.1, Pictar, miRanda, miRTarBase and DAVID databases were used for target gene prediction and enrichment pathway analysis. Results: hsa-miR-214-3p was overexpressed in cervical cancer cells. The overexpression of hsa-miR-214-3p enhanced the proliferation and clonality of cells (P <0.05) hsa-miR-214-3p significantly decreased the proliferation of cells (P <0.001). Flow cytometry showed that the percentage of apoptotic cells in SiHa cells was significantly increased (P <0.05) (P <0.05). The over-expression of hsa-miR-214-3p and the inhibition of endogenous hsa-miR-214-3p expression had no significant effect on the migration of SiHa cells (P> 0.05). Bioinformatics analysis showed that the target gene of hsa-miR-214-3p was mainly enriched in phosphatidylinositol signal system and Wnt signaling pathway. Conclusion: The overexpression of hsa-miR-214-3p can promote the proliferation of cervical cancer cells. Inhibiting the expression of endogenous hsa-miR-214-3p can inhibit the proliferation of SiHa cells and promote the apoptosis of hsa-miR- 3p may regulate the apoptosis process of SiHa cells by regulating the expression of Bcl2 gene. The above results provide new clues for the study of molecular mechanism of cervical cancer and provide a potential target for clinical diagnosis and treatment of cervical cancer.