Open AccessMicroRNA‑505‑3p inhibits development of glioma by targeting HMGB1 and regulating AKT expression
Author(s) -
Zhenlin Cheng,
Bin Wang,
Cheng Zhang
Publication year - 2020
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2020.11714
Subject(s) - microrna , oncogene , protein kinase b , molecular medicine , glioma , cell cycle , cancer research , pi3k/akt/mtor pathway , apoptosis , biology , microbiology and biotechnology , genetics , gene
Previous studies have reported that microRNA (miR)-505 exhibits important effect in human cancers. However, the regulatory mechanism of miR-505-3p/high-mobility group box 1 (HMGB1) axis is still unclear in glioma. Therefore, the regulatory mechanism of miR-505-3p/HMGB1 axis in glioma was illuminated. Expression of miR-505-3p and HMGB1 was observed by RT-qPCR. Protein expression was measured by western blot analysis. Dual luciferase assay was performed to confirm the relationship between miR-505-3p and HMGB1. The function of miR-505-3p was investigated by MTT and Transwell assays. Expression of miR-505-3p was reduced in glioma, which was related to poor clinical outcomes and prognosis in glioma patients. Moreover, overexpression of miR-505-3p suppressed proliferation, migration and invasion of glioma cells. In addition, HMGB1 was confirmed as a direct target of miR-505-3p, and miR-505-3p inhibited the development of glioma by targeting HMGB1. Furthermore, miR-505-3p blocked EMT suppressing p-AKT expression in glioma cells. In conclusion, miR-505-3p inhibited the development of glioma by targeting HMGB1 and regulating AKT expression.