The Effect and Mechanism of Action of Homo Sapiens-microRNA-128 on Cervical Cancer Progression? A Prospective Laboratory Study

Backgrounds: To investigate the effect and its mechanism of homo sapiens-microRNA-128 (hsa-miR-128) on cervical cancer (CC) progression.Methods: Hsa-miR-128 level was measured in CC patients using RT-qPCR (reverse transcription quantitative PCR). CCK-8 (cholecystokinin octapeptide), colony formation, flow cytometry, western blotting, wound healing and transwell assay were used to investigate hsa-miR-128 effects on CC progression. The binding capacity between miR-128a and forkhead box protein 2 (FOXP2) was assessed using the luciferase reporter assay.Results: Hsa-miR-128 expression was significantly lower and FOXP2 level was significantly higher in CC tissues than adjacent normal tissues. Hsa-miR-128 sponged and negatively controlled FOXP2. Hsa-miR-128 targeted FOXP2 to repress proliferation and the cell cycle, while it facilitated apoptosis in TGF-beta (transforming growth factor-beta)-treated CaSki (a human cervical cancer cell line) cells. Additionally, hsa-miR-128 targeted FOXP2 in TGF-beta-treated CaSki cells to decrease cell invasion and migration. Further studies revealed that hsa-miR-128 inactivated the TGF-beta/Smad2/3 pathway by targeting FOXP2 in TGF-beta-treated CaSki cells. Hsa-miR-128 suppressed the development of CC by silencing TGF-beta/Smad2/3 signaling through targeting FOXP2. Conclusions: Hsa-miR-128 suppressed cell proliferation and metastasis of CC through targeting FOXP2, and expedited the apoptosis of CC cells by inhibiting the TGF-beta/Smad2/3 signaling pathway.