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Long non-coding RNA MEG3 suppresses the growth of glioma cells by regulating the miR-96-5p/MTSS1 signaling pathway

机译:长的非编码RNA MEG3通过调节miR-96-5p / MTSS1信号通路抑制神经胶质瘤细胞的生长

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摘要

Glioma is one of the most common types of tumor of the central nervous system with high mobility and mortality. The prognosis of patients with high-grade glioma is poor. Therefore, it is urgent to develop the therapeutic strategies for the treatment of glioma. Long non-coding RNAs (lncRNAs) have been reported as potential inducers or suppressors of numerous types of tumors including glioma. Previous studies have revealed that lncRNA maternally expressed gene 3 (MEG3) is involved in the initiation and progression of cancer; however, the underlying mechanisms remain unclear. In the present study, MEG3 was downregulated in glioma tissue. In addition, downregulation of MEG3 was observed in human glioma cell lines compared with normal astrocyte cells. Furthermore, overexpressed MEG3 inhibited the proliferation, migration and invasion of glioma cells. Additionally, microRNA-96-5p (miR-96-5p) was a promising target of MEG3, and the promoting effects of miR-96-5p on cell growth and metastasis could be reversed by upregulated MEG3. Metastasis suppressor 1 (MTSS1) was predicted as the putative target of miR-96-5p, and its expression was restored by MEG3. In summary, the present data provided novel insight into the roles of MEG3 in glioma, and MEG3/miR-96-5p/MTSS1 signaling could be a promising therapeutic target for the treatment of patients with glioma.
机译:胶质瘤是中枢神经系统最常见的肿瘤类型之一,具有很高的活动性和死亡率。高度神经胶质瘤患者的预后较差。因此,迫切需要开发治疗神经胶质瘤的治疗策略。据报道,长的非编码RNA(lncRNA)是多种类型的肿瘤(包括神经胶质瘤)的潜在诱导物或抑制物。先前的研究表明,lncRNA母源表达基因3(MEG3)参与癌症的发生和发展。但是,其潜在机制仍不清楚。在本研究中,MEG3在神经胶质瘤组织中被下调。另外,与正常星形胶质细胞相比,在人神经胶质瘤细胞系中观察到MEG3的下调。此外,过表达的MEG3抑制神经胶质瘤细胞的增殖,迁移和侵袭。另外,microRNA-96-5p(miR-96-5p)是MEG3的有希望的靶标,而miR-96-5p对细胞生长和转移的促进作用可以通过上调MEG3来逆转。转移抑制因子1(MTSS1)被认为是miR-96-5p的假定靶标,其表达被MEG3恢复。总之,本数据提供了关于MEG3在神经胶质瘤中的作用的新颖见解,并且MEG3 / miR-96-5p / MTSS1信号传导可能是治疗神经胶质瘤患者的有希望的治疗靶标。

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