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.

中文翻译：

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长非编码 RNA TP73-AS1 通过海绵 miR-103a/GALNT7 通路促进神经胶质瘤的发生。


神经胶质瘤是成人中最具侵袭性、最常见的脑肿瘤。长非编码 RNA (lncRNA) 是癌症发展中的基因表达调节因子之一。先前的研究认为，神经胶质瘤中 LncRNA TP73-AS1 (TP73-AS1) 的上调与低存活率有关。然而，LncRNA TP73-AS1在神经胶质瘤中的精确机制仍不清楚。在此，我们发现 TP73-AS1 在神经胶质瘤中表达上调，并与不良预后相关。 TP73-AS1 的沉默抑制了神经胶质瘤细胞的增殖并导致细胞死亡。从机制上讲，我们发现神经胶质瘤中的 TP73-AS1 通过将 miR-103a 与 GALNT7 隔离来充当 ceRNA。此外，本研究的结果揭示了 TP73-AS1 和 miR-103a 之间的相互表达，以及 TP73-AS1 和 GALNT7 之间的正向调节，验证了已确定的机制。此外，荧光素酶报告基因检测确定 miR-103a 是 TP73-AS1 和 GALNT7 的直接结合位点。此外，CCK-8和集落形成测定的结果表明，GALNT7的外源表达逆转了TP73-AS1诱导的神经胶质瘤细胞分裂抑制。总而言之，我们的结果表明，TP73-AS1 通过竞争 TP73-AS1/miR-103a/GALNT7 环中的内源 RNA (ceRNA) 来促进神经胶质瘤的进展。