MicroRNA‑505‑3p inhibits development of glioma by targeting HMGB1 and regulating AKT expression
- Zhenlin Cheng
- Bin Wang
- Cheng Zhang
Affiliations: Department of Neurosurgery, Zhangye People's Hospital Affiliated to Hexi University, Zhangye, Gansu 734000, P.R. China, Department of Neurosurgery, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang 830001, P.R. China
- Published online on: June 9, 2020 https://doi.org/10.3892/ol.2020.11714
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et al. This is an open access article distributed under the
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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.