Glioma is the most common intracranial malignancy and has been recognized as one of the most invasive primary tumors. Although there have been many studies on its growth mechanism, the molecular mechanism for growth inhibition is still unclear. The aim of this study was to show that
microRNA-362-3p inhibits glioma growth by targeting PAX3 and regulating Wnt/beta-catenin pathway. We collected platelets from 12 healthy controls and 8 patients with glioma from the GEO database for comparison. The ncRNA and transcription factors that regulate the module were predicted to
reveal the mechanism of microRNA-362-3p through co-expression module analysis, enrichment analysis, and hypergeometric testing. Two functional modules were obtained by integrating potential pathogenic genes and co-expression analysis. GPATCH4 and MYOD1 genes were expressed differentially and
had active regulatory roles in the dysfunction module; thus, they were identified as key genes for glioma growth. Next, we performed ncRNA pivot and transcription factors (TFs) especially about the pivot analysis. The results showed microRNA-362-3p gene interest that significantly regulated
the dysfunction module. Therefore, we identified microRNA-362-3p as a dysfunctional molecule in the growth process of glioma. MicroRNA-362-3p could inhibit glioma growth by targeting PAX3 and regulating the Wnt/beta-catenin pathway. The inhibition of this pathway may be a new target for the
treatment of glioma. This study improves our understanding of growth inhibition in glioma and provides reference values for the treatment of this disease.
Glioma growth inhibition by neurostatin and O-But GD1b
