Hsa-miR-650 Inhibits NF2-negative Meningioma Growth by Targeting RAC1
10.16476/j.pibb.2023.0349
- VernacularTitle:Hsa-miR-650通过靶向RAC1抑制NF2阴性脑膜瘤的生长
- Author:
Chao ZHANG
1
;
Peng LI
1
;
Bo WANG
1
;
Ying WANG
1
;
Pi-Nan LIU
1
Author Information
1. Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China
- Publication Type:Journal Article
- Keywords:
neurofibromatosis type 2 (NF2);
meningiomas;
hsa-miR-650;
RAC1;
bioinformatics
- From:
Progress in Biochemistry and Biophysics
2024;51(7):1687-1696
- CountryChina
- Language:English
-
Abstract:
ObjectiveThis study aimed to identify a potential miRNA-mRNA axis in neurofibromatosis type 2 (NF2)-negative meningiomas, investigate their target relationships, and determine their biological functions. MethodsThe GSE17792 dataset, which contains data related to NF2-negative meningiomas, was downloaded from the Gene Expression Omnibus (GEO) database. The limma package of R software was used to determine the differentially expressed miRNAs (DeMiRNAs). The miRWalk 2.0 database was applied to obtain the target genes of DeMiRNAs. The Search Tool for the Retrieval of Interacting Genes (STRING) database was utilized to build protein-protein interaction (PPI) networks, and hub genes were identified via Cytoscape software. The expression and biological roles of the screened miRNAs were further validated. ResultsAltogether, 86 DeMiRNAs, consisting of 52 upregulated and 34 downregulated miRNAs, were found in NF2-negative meningioma tumor samples compared with arachnoid tissue controls. Fourteen miRNAs associated with 274 target genes were identified among these DeMiRNAs, and miRNA-target gene networks were constructed based on these data. Analysis with cytoHubba showed that two miRNAs (hsa-miR-650 and hsa-miR-623) were among the top 20 key hub genes in the PPI network. Further qRT-PCR experimental verification suggested that the expression of hsa-miR-650 was significantly higher in NF2-negative meningiomas than in normal brain tissues. Downregulation of hsa-miR-650 inhibited the proliferation and induced the apoptosis of NF2-negative meningioma cells. Finally, RAC1 was identified as a target of hsa-miR-650. ConclusionHsa-miR-650 acts as a tumor promoter and might function as a therapeutic target for patients with NF2-negative meningiomas.
