Abstract
PURPOSE: LncRNA MAFG-AS1 plays critical roles in several types of cancer, while its role in glioblastoma (GBM) is unknown. By analyzing the TCGA dataset, we observed the upregulation of MAFG-AS1 in GBM. This study aimed to investigate the involvement of MAFG-AS1 in GBM cancer. METHODS: The expression levels of MAFG-AS1, mature miR-34a, and miR-34a precursor in GBM and paired non-tumor tissues of 56 GBM patients were determined by RT-qPCR. Correlations are analyzed using linear regression. Overexpression of MAFG-AS1 was achieved in GBM cells, followed by measurement of the expression levels of mature miR-34a, miR-34a precursor, DICER and Drosha by RT-qPCR. The roles of MAFG-AS1 and miR-34a in regulating GBM cell proliferation were evaluated by CCK-8 assay. Flow cytometry was performed to explore the role of MAFG-AS1 and miR-34a in regulating the apoptosis and cell cycle of GBM cells. Cell scratch experiment was performed to determine the role of MAFG-AS1 and miR-34a in regulating the migration of GBM cells. Subcutaneous tumor animal model was used for in vivo study. The expressions levels of BCL-2 and caspase-3 were detected by Western blot analysis. RESULTS: MAFG-AS1 was upregulated in GBM, while mature miR-34a was downregulated in GBM. Interestingly, MAFG-AS1 was inversely correlated with mature miR-34a but not miR-34a precursor across GBM tissues. In GBM tissues, the overexpression of MAFG-AS1 did not affect the expression levels of miR-34a precursor but reduced the expression levels of mature miR-34a. MAFG-AS1 promoted the expression of DICER and Drosha in GBM cells. Moreover, the overexpression of MAFG-AS1 promoted the proliferation of GBM cells and reduced the inhibitory effects of miR-34a on cell proliferation but did not affect cell cycle, apoptosis and migration. The overexpression of MAFG-AS1 promoted the progression of GBM in vivo by promoting the proliferation of GBM cells while miR-34a reversed the effect of overexpression of MAFG-AS1. CONCLUSIONS: MAFG-AS1 may suppress the maturation of miR-34a to promote GBM cell proliferation.