miR-24-3p对宫颈癌细胞增殖与迁移的作用及机制研究

The Effect and Mechanism of miR-24-3p on Proliferation and Migration in Human Cervical Cancer Cells

该文探讨了miR-24-3p对宫颈癌细胞增殖和迁移的促进作用及其机制。采用miR-24-3p抑制剂下调宫颈癌细胞中miR-24-3p的表达后,通过MTT、Transwell实验和Western blot检测细胞增殖、迁移和PCNA蛋白水平;采用生物信息学方法预测miR-24-3p的靶基因并进行功能注释和筛选;双荧光素酶报告实验和Western blot验证靶基因类血管动蛋白-2(angiomotin-like 2,AMOTL2),并通过siRNA抑制AMOTL2检测其对宫颈癌细胞迁移的影响。结果显示,下调miR-24-3p能抑制宫颈癌细胞的增殖和迁移能力并减少PCNA蛋白表达;其靶基因主要存在细胞与细胞连接组分中,显著富集于蛋白激酶活性分子功能、蛋白质自身磷酸化生物学过程和癌症中microRNA信号通路;miR-24-3p能靶向负调控最佳靶基因AMOTL2,下调AMOTL2可促进宫颈癌细胞CaSki的迁移。总之,miR-24-3p可调控多靶基因参与多个生物学过程和多条信号通路,在宫颈癌中可促进细胞增殖且通过靶向AMOTL2促进迁移。

This study aimed to investigate the role of miR-24-3p in the proliferation and migration of cervical cancer cells and its mechanism.miR-24-3p inhibitors were used to down-regulate the expression of miR-24-3p in cervical cancer cells,then MTT Transwell assays and Western blot were used to measure cell proliferation,migration and the protein level of the proliferating cell nuclear antigen.The target genes of miR-24-3p were predicted and then used for function annotation through bioinformatic methods.The relationship between miR-24-3p and target gene AMOTL2(angiomotin-like 2)was verified by dual-luciferase reporter system and Western blot,siRNA inhibited AMOTL2 was used to detect its effect on cervical cancer cell migration.Data showed that down-regulating miR-24-3p could inhibit the proliferation and migration ability of cervical cancer cells and reduce PCNA protein expression.Its target genes were mainly present in the cell-cell junction component,and were significantly enriched in biological processes including protein kinase activity molecular function,proteins autophosphorylation and microRNA in cancer signaling pathway.miR-24-3p was a negative regulator of the optimal target gene AMOTL2,and the decreased expression of AMOTL2 promoted the migration of cervical cancer cell CaSki.In conclusion,miR-24-3p can regulate multiple target genes,which are involved in varied biological processes and signaling pathways,also promote cell proliferation and facilitate cell migration by targeting AMOTL2 in cervical cancer.