Third Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, P.R. China.
Department of Neurosurgery, People's Hospital of Inner Mongolia Autonomous Region, Hohhot, Inner Mongolia, P.R. China.
Biosci Rep. 2021 Jul 30;41(7). doi: 10.1042/BSR20200767.
Glioma is the most common malignant tumor in the human central nervous system. Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes oncogenesis in various tumors. In the present study, we aimed to examine the role of NEAT1 in altering the properties of gliomas.
Quantitative real-time PCR technology was used to determine the expression levels of relevant genes in tumor tissues and cell lines. The protein expression levels were validated by Western blotting. Cell counting kit-8 (CCK-8) and colony formation assays were used to test the cell proliferation ability. A luciferase reporter assay was used to determine the interactions of the genes. Tumor xenografts were used to detect the role of NEAT1 in gliomas in vivo.
We demonstrated that NEAT1 up-regulated glioma cells and negatively correlated with miR-98-5p in glioma tissues. A potential binding region between NEAT1 and miR-98-5p was confirmed by dual-luciferase assays. NEAT1 knockdown inhibited glioma cell proliferation. The inhibition of miR-98-5p rescued the knockdown of NEAT1 in glioma cells. Basic leucine zipper and W2 domain containing protein 1 (BZW1) was identified as a direct target of miR-98-5p. We also identified that BZW1 was positively correlated with NEAT1 in glioma tissues. NEAT1 knockdown inhibited glioma cell proliferation in vivo via miR-98-5p/BZW1.
Our results suggest that NEAT1 plays an oncogenic function in glioma progression. Targeting NEAT1/miR-98-5p/BZW1 may be a novel therapeutic treatment approach for glioma patients.
神经胶质瘤是人类中枢神经系统中最常见的恶性肿瘤。长链非编码 RNA 核斑浆组装转录本 1（NEAT1）在多种肿瘤中促进肿瘤发生。在本研究中，我们旨在研究 NEAT1 改变神经胶质瘤特性的作用。
采用定量实时 PCR 技术检测肿瘤组织和细胞系中相关基因的表达水平。采用 Western blot 验证蛋白表达水平。细胞计数试剂盒-8（CCK-8）和集落形成实验用于检测细胞增殖能力。采用荧光素酶报告基因实验确定基因的相互作用。肿瘤异种移植用于检测 NEAT1 在体内对神经胶质瘤的作用。
我们证明，NEAT1 上调神经胶质瘤细胞，与神经胶质瘤组织中的 miR-98-5p 呈负相关。双荧光素酶报告基因实验证实了 NEAT1 和 miR-98-5p 之间的潜在结合区域。NEAT1 敲低抑制神经胶质瘤细胞增殖。miR-98-5p 的抑制挽救了神经胶质瘤细胞中 NEAT1 的敲低。碱性亮氨酸拉链和 W2 结构域包含蛋白 1（BZW1）被鉴定为 miR-98-5p 的直接靶标。我们还发现，BZW1 与神经胶质瘤组织中的 NEAT1 呈正相关。NEAT1 敲低通过 miR-98-5p/BZW1 抑制体内神经胶质瘤细胞增殖。
我们的结果表明，NEAT1 在神经胶质瘤进展中发挥致癌作用。靶向 NEAT1/miR-98-5p/BZW1 可能是神经胶质瘤患者的一种新的治疗方法。
