Abstract

Background: Glioma is one of the most common brain tumors. Copious microRNAs have been identified as critical regulators in the development of glioma. MicroRNA-142-3p (miR-142-3p) has been reported as a tumor suppressor in some malignancies. However, the roles and molecular mechanisms of miR-142-3p in the development of glioma are poorly defined. Methods: An RT-qPCR assay was carried out to detect expressions of miR-142-3p and high-mobility group box 1 (HMGB1) mRNA. A bioinformatic analysis and a luciferase reporter assay were used to explore the interaction between miR-142-3p and HMGB1 3’UTR. A Western blot assay was performed to examine protein expression of HMGB1, c-myc, cleaved caspase-3, and β-catenin. Cell proliferative ability was assessed by an MTS assay. The cell apoptotic rate was measured using flow cytometry via the double-staining of Annexin V-FITC and propidium iodide (PI). Results: MiR-142-3p expression was remarkably reduced in glioma tissues. Mechanical analyses showed that HMGB1 was a target of miR-142-3p. Functional investigations revealed that miR-142-3p suppressed proliferation and induced apoptosis by targeting HMGB1 in glioma cells. Moreover, miR-142-3p inactivated Wnt/β-catenin signaling and activated caspase-3 signaling by targeting HMGB1 in glioma cells. Conclusion: MiR-142-3p inhibits proliferation and induces apoptosis by targeting HMGB1 via the Wnt/β-catenin signaling pathway in glioma cells, providing a deep exploration into the roles and molecular basis of miR-142-3p in the proliferation and apoptosis of glioma cells and highlighting the therapeutical values of miR-142-3p and HMGB1 for glioma.