Purpose: To explore the biological function of micro ribonucleic acid (miR)-200a in cervical cancer (CC).
Methods: HeLa cells were transfected with miR-200a inhibitor or negative control (NC). Next, the effects of miR-200a down-regulation on the proliferation of CC cells were detected via methyl thiazolyl tetrazolium (MTT) assay and colony formation assay. Subsequently, flow cytometry was performed to determine the role of miR-200a in regulating the apoptosis of CC cells. Finally, Western blotting was conducted to detect the effects of miR-200a on the hypoxia-inducible factor 1-alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway.
Results: RT-qPCR results confirmed that miR-200a was significantly down-regulated in HeLa cells transfected with miR-200a inhibitor compared with those transfected with NC (p<0.05). Besides, in comparison with cells in NC group, HeLa cells with down-regulated miR-200a showed weakened proliferation ability (p<0.05) and a remarkably decreased colony number (p<0.05). Moreover, flow cytometry results manifested that the down-regulation of the miR-200a expression level obviously promoted cell apoptosis (p<0.05). Furthermore, western blotting analyses also confirmed that the protein expression levels of HIF-1α and VEGF were increased after miR-200a overexpression.
Conclusions: MiR-200a facilitates the proliferation of CC cells and activates the HIF-1α/VEGF signaling pathway by targeting EGLN1.