MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway

Abstract

BackgroundCervical cancer (CC) is frequently diagnosed, and accounts for a large proportion of cancer-related mortality worldwide. Therefore, it is an urgent need to explore the mechanisms of CC progression and seek new therapeutic targets. We know that microRNA-137 (miR-137) is involved in CC progression; however, it’s mechanism in CC has not yet been clarified.MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expressions of miR-137 and Notch homolog 1 messenger RNA (Notch1 mRNA) in CC cells. Cell Counting Kit-8 (CCK-8) and Transwell assay were utilized to monitor the proliferation, invasion, and migration of CC cells. The binding relationship of miR-137 with Notch1 was detected by dual luciferase reporter gene assay. Western blot was used to determine the expressions of Notch1, p-AKT/AKT, and p-mTOR/mTOR signaling pathways.ResultsThe results showed that miR-137 was down-regulated and Notch1 was up-regulated in CC cells. MiR-137 was reversely correlated with Notch1, and Notch1 partially reversed the promotion of miR-137 silencing on malignant phenotype of CC cells. Furthermore, in vitro experiments confirmed that miR-137 partially impeded CC progression via regulation of the Notch1 and PI3K/AKT/mTOR axis.ConclusionsMiR-137 targets Notch1 and regulates CC through the PI3K/Akt/mTOR pathway. The miR-137/Notch1 axis may be a promising target for CC patients, and these findings can provide a reference for the clinical treatment of CC.