MiR-628-5p Inhibits Cervical Carcinoma Proliferation and Promotes Apoptosis by Targeting VEGF

Background: It has been reported that the dysregulation of microRNAs (miRNAs) is implicated in the biological processes of diverse diseases, including the tumorigenesis of human cancers. MicroRNA-628-5p (miR-628-5p) is differentially expressed and plays a critical role in several cancers, but the role of miR-628-5p in cervical cancer has not been well studied. Methods: The TCGA database and RT-qPCR were used to evaluate the expression profile of miR-628-5p in cervical cancer tissues. Transfection efficiency of synthetic miRNAs was detected using RT-qPCR. The biological effects of miR-628-5p on cervical cancer cells were assessed by the CCK-8 assay, flow cytometry, western blot analysis, and the tube formation assay. The expression levels of key proteins involved in cell apoptosis, the cell cycle and the PI3K pathway were analyzed by western blot analysis. Bioinformatic analysis and the luciferase reporter assay were performed to investigate the targeted relationship between miR-628-5p and vascular endothelial growth factor (VEGF). Results: MiR-628-5p was downregulated and negatively correlated with Ki-67 expression in cervical cancer tissues, and its low level predicted poor survival of patients. Functional assays indicated that miR-628-5p inhibited cell proliferation and promoted cell apoptosis. Mechanically, VEGF was verified to be a downstream target of miR-628-5p. Moreover, overexpression of VEGF could reverse the effects of miR-628-5p on VEGF/PI3K/AKT signaling, cell proliferation, apoptosis, the cell cycle and angiogenesis in cervical cancer. Conclusions: MiR-628-5p inhibited cervical cancer cell proliferation and promoted apoptosis by targeting VEGF.