Osthole inhibited cell proliferation and induced cell apoptosis through decreasing CPEB2 expression via up-regulating miR-424 in endometrial carcinoma

Abstract

Objective: Endometrial carcinoma (EC) was the fourth female malignancies in developed countries. Given that the prognosis of EC is extremely poor, it is vital to investigate its pathogenesis and effective therapeutic targets. However, the mechanism of osthole in EC remains unknown.Materials and methods: Firstly, the different doses of osthole (0, 50, 100, and 200 μM) were used to treat the Ishikawa and KLE cells. The cell proliferation, apoptosis, and cell cycle were measured by cell counting kit-8 (CCK-8), Annexin V-FITC/PI, and cell cycle assays. The apoptosis-related protein levels were examined by western blot. The miR-424 levels in Ishikawa and KLE cells were assessed by quantitative RT-PCR (qRT-PCR). Also, the binding of miR-424 and cytoplasmic polyadenylation element binding protein 2 (CEPB2) was detected by the luciferase reporter assay.Results: In this study, the increasing dose of osthole inhibited proliferation and induced apoptosis of Ishikawa and KLE cells. Moreover, the increasing dose of osthole up-regulated miR-424 and down-regulated the expression of CPEB2. CPEB2 was proved to be the target gene of miR-424. Interestingly, the over-expression of CPEB2 could reverse the changes of osthole-induced proliferation and apoptosis of Ishikawa and KLE cells.Conclusions: In summary, we provided first evidences that osthole inhibited proliferation and induced apoptosis through up-regulating miR-424 to inhibit expression of CPEB2 in EC. Our findings indicated that osthole might act as a novel and potential therapeutic agent for the treatment of EC.