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Research Paper|Volume 15, Issue 12|pp 5412—5425

Tumor-suppressive function and mechanism of miR-873-5p in glioblastoma: evidence based on bioinformatics analysis and experimental validation

Xiaobin Zhang1, Fangkun Jing2, Chen Guo1, Xinning Li1, Jianan Li1, Guobiao Liang1
  • 1Department of Neurosurgery, General Hospital of the Northern Theater Command of Chinese People’s Liberation Army, Shenyang 110000, China
  • 2Department of Neurosurgery, Jinqiu Hospital of Liaoning Province, Shenyang 110000, China
* Co-first authors
Received: February 27, 2023Accepted: May 16, 2023Published: June 28, 2023
https://doi.org/10.18632/aging.204800

Copyright: © 2023 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

This study aims to clarify the mechanistic actions of microRNA-873-5p (miR-873-5p) on glioblastoma (GBM) progression. The most differentially expressed miRNAs were retrieved from the GEO database. It was established that miR-873-5p was downregulated in GBM tissues and cells. Based on in silico prediction and experimental data, HMOX1 was demonstrated to be a target gene of miR-873-5p. Further, miR-873-5p was then ectopically expressed in GBM cells to examine its effect on the malignant behaviors of GBM cells. Overexpression of miR-873-5p inhibited GBM cell proliferation and invasion by targeting HMOX1. HMOX1 promoted SPOP expression by increasing HIF1α expression, thus stimulating GBM cell malignant phenotypes. miR-873-5p suppressed the malignant phenotypes of GBM cells and tumorigenesis in vitro and in vivo by inhibiting the HMOX1/HIF1α/SPOP signaling axis. This study uncovers a novel miR-873-5p/HMOX1/HIF1α/SPOP axis in GBM, providing new insights into GBM progression and therapeutic targets for GBM treatment.