miR-214 targets the PTEN-mediated PI3K/Akt signaling pathway and regulates cell proliferation and apoptosis in ovarian cancer

The present study aimed to investigate the potential role of microRNA (miR)-214 in targeting the phosphatase and tensin homolog (PTEN)-mediated phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in ovarian cancer (OC). The target gene of miR-214 was determined by luciferase reporter gene assay and was indicated to be PTEN. Human SK-OV-3 cells were transfected with a miR-214 inhibitor and a miR-214 mimic, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect relative expression of miR-214. The MTT assay was performed to detect cell viability following transfection. Cell cycle and apoptosis were assessed by staining with propidium iodide (PI) and double staining with Annexin V/PI, respectively. The expression levels of PTEN and PI3K/Akt signaling pathway-associated proteins were detected by western blot analysis. The expression of miR-214 in tumor tissues and normal tissues was detected by RT-qPCR, and PTEN expression was detected by immunohistochemistry. SK-OV-3 cells transfected with a miR-214 inhibitor showed significantly inhibited cell viability and proliferation, and markedly increased apoptotic rate. SK-OV-3 cells transfected with miR-214 mimic showed significantly increased viability and proliferation, and markedly decreased apoptotic rate. The cells transfected with a miR-214 inhibitor exhibited significantly upregulated PTEN expression and significantly downregulated phosphatidylinositol (3,4,5)-trisphosphate (PIP3), phosphorylated (p)-Akt and p-glycogen synthase kinase (GSK)-3 beta expression. The cells transfected with miR-214 mimic exhibited significantly downregulated PTEN expression and significantly upregulated PIP3, p-Akt and p-GSK-3 beta expressions. The OC tissues exhibited an increased expression of miR-214 and a reduced positive rate of PTEN expression compared with adjacent normal tissues. miR-214 may activate the PI3K/Akt signaling pathway by downregulating the targeted PTEN, which may promote OC cell proliferation and inhibit apoptosis.