Evidence has revealed that long non-coding RNAs (lncRNAs) are involved in carcinogenesis and tumor progression. lncRNAs play an important role in regulation of numerous cellular processes including cell proliferation, apoptosis, cell cycle, differentiation, and motility. Several studies have demonstrated that lncRNA EPIC1 governs cell growth, cell cycle, migration, invasion, and drug resistance in human malignancies. However, the role of EPIC1 and its underlying molecular mechanisms in glioma have not been investigated. In this study, we determined the function of EPIC1 in glioma cells via upregulation or downregulation of EPIC1. We further dissected the mechanism of EPIC1-mediated tumor progression in glioma. Our results showed that inhibition of EPIC1 suppressed cell viability, induced apoptosis, inhibited cell invasion, and increased cell sensitivity to temozolomide in glioma cells. Consistently, overexpression of EPIC1 exhibited the opposite effects in glioma cells. Moreover, our data suggest that EPIC1 exerts its biological functions via targeting Cdc20 in glioma cells. In line with this, overexpression of Cdc20 reversed the EPIC1-mediated tumor progression in glioma cells. Therefore, targeting EPIC1 might be a useful approach for glioma treatment.

有证据表明，长的非编码RNA（lncRNA）参与了癌变和肿瘤的发展。lncRNA在许多细胞过程的调控中起着重要作用，包括细胞增殖，凋亡，细胞周期，分化和运动。多项研究表明，lncRNA EPIC1可以控制人类恶性肿瘤的细胞生长，细胞周期，迁移，侵袭和耐药性。但是，尚未研究EPIC1在神经胶质瘤中的作用及其潜在的分子机制。在这项研究中，我们通过上调或下调EPIC1来确定EPIC1在神经胶质瘤细胞中的功能。我们进一步解剖了神经胶质瘤中EPIC1介导的肿瘤进展的机制。我们的结果表明，抑制EPIC1可抑制细胞活力，诱导细胞凋亡，抑制细胞侵袭，并增加了对胶质瘤细胞中替莫唑胺的细胞敏感性。一致地，EPIC1的过表达在神经胶质瘤细胞中表现出相反的作用。此外，我们的数据表明EPIC1通过靶向胶质瘤细胞中的Cdc20发挥其生物学功能。与此相符，Cdc20的过表达逆转了EPIC1介导的神经胶质瘤细胞中的肿瘤进展。因此，靶向EPIC1可能是治疗神经胶质瘤的有用方法。