Abstract

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)‑3β expression. The cells transfected with miR‑214 mimic exhibited significantly downregulated PTEN expression and significantly upregulated PIP3, p‑Akt and p‑GSK‑3β 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 prolife