Emerging evidence underlined the crucial roles played by long non-coding RNAs (lncRNAs) in glioma. MINCR has been reported in multiple malignancies. Here, we studied its function and potential mechanism in glioma, which remain unclear. Gene expressions were analyzed by qRT-PCR assay. Both in vitro and in vivo assays were conducted to evaluate the cellular function of MINCR in glioma. The subcellular situation of MINCR was detected by subcellular fractionation and FISH assays. Luciferase reporter, RNA pull-down and RNA immunoprecipitation (RIP) assays were combined to investigate potential mechanisms of relevant genes. MINCR was up-regulated in glioma. MINCR depletion markedly refrained glioma cell proliferation, migration and invasion via sponging miR-876-5p. MiR-876-5p suppressed the malignant behaviors of glioma via binding to GSPT1. MINCR shared the binding sites with the 3’-untranslated region of GSPT1 and prevented the binding of miR-876-5p to GSPT1 mRNA, thus up-regulating the level of GSPT1. Moreover, miR-876 inhibition and GSPT1 up-regulation counteracted the functional effect induced by silencing MINCR on glioma progression. Our findings uncovered that MINCR might aggravated glioma cell proliferation and migration via acting as competing endogenous RNA (ceRNA), indicating prospective novel therapeutic target for glioma.

越来越多的证据强调了长非编码RNA（lncRNA）在神经胶质瘤中所起的关键作用。MINCR已报道有多种恶性肿瘤。在这里，我们研究了其在神经胶质瘤中的功能和潜在机制，目前尚不清楚。通过qRT-PCR测定法分析基因表达。进行了体外和体内试验以评估MINCR在神经胶质瘤中的细胞功能。MINCR的亚细胞情况通过亚细胞分级分离和FISH分析来检测。萤光素酶记者，RNA下拉和RNA免疫沉淀（RIP）分析相结合，以调查相关基因的潜在机制。MINCR在神经胶质瘤中上调。MINCR耗竭通过抑制miR-876-5p显着抑制了胶质瘤细胞的增殖，迁移和侵袭。MiR-876-5p通过与GSPT1结合抑制神经胶质瘤的恶性行为。MINCR与GSPT1的3'非翻译区共享结合位点，并阻止了miR-876-5p与GSPT1 mRNA的结合，从而上调了GSPT1的水平。而且，miR-876抑制和GSPT1上调抵消了MINCR沉默对神经胶质瘤进展所诱导的功能作用。我们的研究结果发现，MINCR可能通过竞争内源性RNA（ceRNA）加剧神经胶质瘤细胞的增殖和迁移，这表明神经胶质瘤有望成为新型治疗靶标。