RESUMEN
Glioma is the most aggressive, commonly occurring brain tumor in adults. Long non-coding RNAs (lncRNAs) are among the gene expression regulators in cancer development. Previous research posited that the up-regulation of LncRNA TP73-AS1 (TP73-AS1) in glioma is linked to low survival rates. However, the precise LncRNA TP73-AS1 mechanism in glioma remains unknown. Herein, we found that TP73-AS1 was up-regulated in glioma and was associated with a dismal prognosis. The silencing of TP73-AS1 repressed the multiplication of glioma cells and caused cell death. Mechanistically, we identified that TP73-AS1 in glioma acts as a ceRNA by sequestering miR-103a from GALNT7. Further, the results of this study revealed a reciprocal expression between TP73-AS1 and miR-103a, and a positive regulation between TP73-AS1 and GALNT7, validating the identified mechanism. Besides, luciferase reporter assay identified miR-103a as the direct binding site of both TP73-AS1 and GALNT7. Moreover, the findings of CCK-8 and colony-formation assays indicated that exogenous expression of GALNT7 reversed TP73-AS1-induced division inhibition of glioma cells. Altogether, our results established that TP73-AS1 facilitates the progression of glioma through competing for endogenous RNA (ceRNA) in a TP73-AS1/miR-103a/GALNT7 loop.