MicroRNA‑130a‑3p promotes the proliferation and inhibits the apoptosis of cervical cancer cells via negative regulation of RUNX3.

Aberrant expression of microRNAs (miRs) has been reported in various types of cancer. The aim of the present study was to investigate the role and underlying molecular mechanism of miR‑130a‑3p in cervical cancer (CC). The expression of miR‑130a‑3p in CC tissues and cell lines (CaSki and SiHa) was measured via reverse transcription‑quantitative PCR. SiHa and CaSki cells were transfected with miR‑130a‑3p mimics and a miR‑130a‑3p inhibitor, respectively. The proliferation, apoptosis and migration and invasion abilities of CC cells were then measured using MTT, flow cytometry, wound‑healing and Transwell assays, respectively. TargetScan and dual‑luciferase reporter gene assays were performed to analyze the association between miR‑130a‑3p and its predicted target gene Runt‑related transcription factor 3 (RUNX3). In addition, a xenograft tumor model was established in mice to evaluate the impact of miR‑130a‑3p on tumor growth in vivo. The expression of miR‑130a‑3p was markedly upregulated in CC tissues and cell lines compared with normal tissues and cells. Transfection with miR‑130a‑3p mimics significantly promoted the proliferation, migration and invasion, and inhibited the apoptosis of SiHa cells. Treatment of CaSki cells with a miR‑130a‑3p inhibitor resulted in opposite effects to those of miR‑130a‑3p mimics. RUNX3 was identified as the target gene of miR‑130a‑3p, and overexpression of RUNX3 eliminated the tumor‑promoting effect of miR‑130a‑3p mimics on CC cells. Overexpression of miR‑130a‑3p also promoted tumor growth in mice. In conclusion, miR‑130a‑3p promoted proliferation, migration and invasion, and inhibited the apoptosis of CC cells via targeting RUNX3, suggesting a novel treatment target for CC.