Glioblastoma is one of the most frequent and aggressive primary tumor of glial brain tumors. Long non-coding RNA Prostate cancer-associated ncRNA transcript 6 (PCAT6) has been identified to influence the progression of many cancers, but its expression and functions in glioblastoma remain unclear. In this study, we intended to investigate the expression, functions and the corresponding mechanisms of PCAT6 in glioblastoma. We observed that PCAT6 expression was upregulated in glioblastoma tissues and cell lines and its high expression was due to the transcriptional activation by Yin Yang 1. miR-513 was a target of PCAT6 and Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) was a target of miR-513. Hence, PCAT6 upregulated IGF2BP1 expression via miR-513 in a competing endogenous RNAs manner. PCAT6 and IGF2BP1 functioned as oncogenes while miR-513 acted as a tumor suppressor gene in glioblastoma. PCAT6 and miR-513 modulated the proliferation and survival of glioblastoma cells via AKT signaling by mediating IGF2BP1. IGF2BP1 raised the expression of PCAT6 by increasing its stability. In conclusion, our results indicate that PCAT6/miR-513/IGF2BP1 positive feedback loop plays a crucial role in facilitating glioblastoma progression.

胶质母细胞瘤是神经胶质脑肿瘤中最常见，最具侵袭性的原发性肿瘤之一。已经确定了长的非编码RNA前列腺癌相关的ncRNA转录本6（PCAT6）影响许多癌症的进展，但是在胶质母细胞瘤中其表达和功能尚不清楚。在这项研究中，我们打算调查PCAT6在胶质母细胞瘤中的表达，功能和相应的机制。我们观察到，胶质母细胞瘤组织和细胞系中PCAT6表达上调，其高表达归因于阴阳1的转录激活。miR-513是PCAT6的靶标，胰岛素样生长因子2 mRNA结合蛋白1（IGF2BP1）则是靶标。 miR-513的目标。因此，PCAT6通过miR-513以竞争性内源RNA的方式上调了IGF2BP1的表达。在成胶质细胞瘤中，PCAT6和IGF2BP1充当癌基因，而miR-513充当肿瘤抑制基因。PCAT6和miR-513通过介导IGF2BP1通过AKT信号传导调节胶质母细胞瘤细胞的增殖和存活。IGF2BP1通过增加其稳定性来提高PCAT6的表达。总之，我们的结果表明PCAT6 / miR-513 / IGF2BP1阳性反馈环在促进胶质母细胞瘤进展中起着至关重要的作用。