Long noncoding RNA SNHG12 facilitates the tumorigenesis of glioma through miR-101-3p/FOXP1 axis

The increasing vital roles of long coding RNA (lncRNAs) in the glioma tumorigenesis have renewedly and roundly recognized. Nevertheless, the in-depth that lncRNAs modulate the gliomagenesis is still elusive. In this research, we focus on the functional study of lncRNA SNHG12 in the glioma pathogenesis. SNHG12 expression was enhanced and high-expressed in the glioma clinical tissue samples and cell lines, especially in the advanced clinical grade. In functional study, knockdown of SNHG12 impaired the proliferation, induced the apoptosis in vitro and, meanwhile, inhibited the tumor growth in vivo. In mechanistic study, it was found that SNHG12 harbored the complementary binding sites with miR-101-3p at 3'-UTR, acting as a miRNA 'sponge'. Furthermore, miR-101-3p also targeted the 3'-UTR of FOXP1 mRNA. The three elements construct the SNHG12/miR-101-3p/FOXP1 axis. Overall, we confirmed a functional regulatory pathway that SNHG12 and miR-101-3p regulated the expression of FOXP1 in glioma cells, forming the SNHG12/miR-101-3p/FOXP1 pathway. This finding might act as a valuable target for glioma.