MicroRNA‑17 downregulates expression of the PTEN gene to promote the occurrence and development of adenomyosis

The aim of the current study was to evaluate the expression of microRNA (miR)‑17 in the endometrial tissues of patients with adenomyosis (AM) and determine its biological function in the occurrence and development of the disease. A total of 45 fresh endometrial tissues of AM patients and 32 normal endometrial tissues were collected from healthy controls. The expression of miR‑17 was evaluated using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The miR‑17‑targeting gene phosphatase and tensin homolog (PTEN) was predicted using bioinformatics and its expression was evaluated with RT‑qPCR and western blot analysis. Endometrial cells were isolated from patients with AM and healthy controls. They were cultured in vitro and transfected with antagomiR‑17 to downregulate miR‑17 expression, subsequently cell viability and apoptosis were measured using MTT and flow cytometry. The expression of PTEN and cell cycle‑ and apoptosis‑related proteins were evaluated using western blot analysis. Endometrial cells that stably overexpressed PTEN were screened in vitro by co‑culture with G418. A dual‑luciferase reporter assay was conducted to verify whether miR‑17 was directly bound to PTEN mRNA. The results demonstrated that expression of miR‑17 was significantly increased in the endometrial tissues of patients with AM compared with control patients (P<0.05). PTEN mRNA and protein expression were significantly lower in the AM group compared with the control group (P<0.05). When the expression of miR‑17 in the cells was downregulated, the expression of PTEN was significantly increased (P<0.05). In addition, expression of Bcl‑2 protein was significantly decreased and that of Bax protein significantly increased compared with the negative control (both P<0.05). The expression of cyclins E1 and D1 were also significantly downregulated (P<0.05). When PTEN was overexpressed or miR‑17 was downregulated, the viability of endometrial cells significantly decreased and cell apoptosis significantly increased (all P<0.05). A dual‑luciferase reporter assay indicated that miR‑17 could directly bind to the PTEN mRNA 3'‑untranslated region to regulate its expression. Thus the current study indicates that expression of miR‑17 was increased in the endometrial tissues of patients with AM and may influence cell apoptosis and cyclin expression through the targeted regulation of PTEN. These results suggest that miR‑17 promotes the occurrence and development of AM.