Mir-145 Inhibits Cervical Cancer Progression And Metastasis By Targeting Wnt2b By Wnt/Beta-Catenin Pathway

Background: Cervical cancer is a very serious female disease worldwide, especially in developing countries. The expression level of miRNA-145 has been revealed to be decreased in various cancers, including cervical cancer. However, the molecular mechanisms by which miR-145 inhibits tumor growth and induces apoptosis in cervical cancer remain unclarified. Methods: The mRNA expression levels of miR-145 and WNT2B were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-145 on cervical cancer proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Transwell assay was conducted to measure cell migration and invasion. Cell apoptosis was examined by flow cytometry assay. The target of miR-145 was predicted by online database and verified by luciferase reporter assay. In vivo experiment was employed to clarify the effect of miR-145 on tumor growth. Results: The expression level of miR-145 was down-regulated while WNT2B expression was up-regulated in cervical cancer cell tissues and cell lines. MiR-145 suppressed cell proliferation, migration and invasion, inhibited Epithelial-Mesenchymal Transition (EMT) process and induced apoptosis. We confirmed that miR-145 weakened WNT2B expression by binding with WNT2B. Furthermore, over-expression of WNT2B reversed the inhibition effects on miR-145 on proliferation and metastasis as well as promoted effects on apoptosis of cervical cells. In addition, we demonstrated that upregulation of miR-145 repressed the Wnt/beta-catenin signaling pathway by repressing WNT2B expression in cervical cancer cells. Conclusion: MiR-145 inhibits cervical cancer progression and metastasis through inactivating Wnt/beta-catenin pathway by targeting WNT2B.