Abstract
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.