The inhibitory effect of long intergenic non-coding RNA 00320 (LINC00320) in glioma cell proliferation has been proposed in a recent study. However, the mechanisms by which LINC00320 regulate aquaporin 9 (AQP9) in glioma require further exploration. Hence, this study aims to investigate effects of LINC00320 on tumorigenicity of glioma cells and angiogenesis of microvascular endothelial cells (MVECs). Expression of LINC00320 and AQP9 in glioma tissues and cells was measured by reverse transcription–quantitative polymerase chain reaction and Western blot analysis. The relationship among LINC00320, nuclear factor κB subunit 1 (NFKB1) and AQP9 was examined by RNA immunoprecipitation, dual-luciferase reporter gene, and chromatin immunoprecipitation assays. The participation of LINC00320 and AQP9 in glioma cell proliferation and MVEC angiogenesis was analyzed using gain- and loss-of-function approaches. Finally, a nude mouse orthotopic xenograft model of glioma was established to investigate the effects of LINC00320 and AQP9 on glioma growth in vivo. LINC00320 was under-expressed and AQP9 was over-expressed in glioma tissues. Further mechanistic investigation showed that LINC00320 downregulated AQP9 by inhibiting the recruitment of NFKB1 to the promoter region of AQP9. LINC00320 overexpression or AQP9 silencing inhibited the proliferation of glioma cells and angiogenesis of MVECs. Also, upregulation of LINC00320 restrained tumor growth and angiogenesis in xenograft mice by downregulating AQP9. Taken together, LINC00320 acts as a tumor suppressor in glioma, thus presenting a novel therapeutic target.

最近的一项研究提出了长基因间非编码 RNA 00320 (LINC00320) 对胶质瘤细胞增殖的抑制作用。然而，LINC00320 在胶质瘤中调节水通道蛋白 9 (AQP9) 的机制需要进一步探索。因此，本研究旨在研究 LINC00320 对胶质瘤细胞致瘤性和微血管内皮细胞 (MVEC) 血管生成的影响。通过逆转录-定量聚合酶链反应和蛋白质印迹分析测量胶质瘤组织和细胞中 LINC00320 和 AQP9 的表达。通过 RNA 免疫沉淀、双荧光素酶报告基因和染色质免疫沉淀测定检查了 LINC00320、核因子 κB 亚基 1 (NFKB1) 和 AQP9 之间的关系。使用增益和功能丧失方法分析 LINC00320 和 AQP9 在胶质瘤细胞增殖和 MVEC 血管生成中的参与。最后，建立了胶质瘤裸鼠原位异种移植模型，研究LINC00320和AQP9对胶质瘤生长的影响。体内. LINC00320 在胶质瘤组织中表达不足，AQP9 过度表达。进一步的机制研究表明，LINC00320 通过抑制 NFKB1 募集到 AQP9 的启动子区域来下调 AQP9。LINC00320 过表达或 AQP9 沉默抑制了胶质瘤细胞的增殖和 MVEC 的血管生成。此外，LINC00320 的上调通过下调 AQP9 抑制了异种移植小鼠的肿瘤生长和血管生成。总之，LINC00320 在胶质瘤中充当肿瘤抑制因子，从而呈现出一种新的治疗靶点。