miR-217 inhibits the migration and invasion of HeLa cells through modulating MAPK1

MicroRNA (miR)-217 serves a pivotal role in the progression of colorectal cancer, renal cell carcinoma and glioma, however, the role of miR-217 in cervical cancer (CC) remains unclear. In the present study, the mechanism of miR-217 in cervical cancer was explored. The mRNA expression of miR-217 and mitogen-activated protein kinase 1 (MAPK1) were assessed using reverse transcription-quantitative polymerase chain reaction analysis. Cell Counting-Kit 8, wound-healing and Transwell assays were performed to detect cell viability, migration and invasion, respectively. Apoptosis and cell cycle were determined by flow cytometry. TargetScan 7.2 and dual-luciferase reporter assays were respectively used to determine miR-217 target genes and their binding capacities. The protein expression levels of MAPK1, phosphorylated (p)-extracellular signal-regulated kinase 1/2 (ERK1/2)/ERK1/2, Bcl-2, Bax and cleaved caspase-3 were quantified by western blotting. It was found that miR-217 was downregulated in patients with CC and in CC cells. The viability, migration and invasion of cells were suppressed by a miR-217 mimic. It was also found that apoptosis was increased and cell cycle was inhibited by the miR-217mimic, which was supported by changes in Bcl-2, Bax and cleaved caspase-3. MAPK1 was upregulated in patients with CC and was a target gene of miR-217. MAPK1 reversed the inhibition of miR-217 on cell viability, migration, invasion and apoptosis. The protein levels of MAPK1 and p-ERK1/2, which were higher in the mimic MAPK1 group than those in the control or mimic groups, were ameliorated by PD98059. The results of the present study demonstrated that miR-217 had an anti-CC effect and may be effectively used in the treatment of CC.