Tianjin Neurosurgical Institute, Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative Diseases, Tianjin Huanhu Hospital, Tianjin, 300350, PR China.
Tianjin Neurosurgical Institute, Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative Diseases, Tianjin Huanhu Hospital, Tianjin, 300350, PR China; Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin, 300350, PR China.
Cancer Lett. 2022 Jan 28;525:33-45. doi: 10.1016/j.canlet.2021.10.033. Epub 2021 Oct 30.
Long noncoding RNAs (lncRNAs) have been shown to be closely related to cancer progression and therapy. However, the clinical significance of lncRNAs and the mechanisms by which they function in glioma are largely unknown. In this study, using online data sets combined with collected clinical glioma tissues, we determined that the lncRNA KB-1460A1.5 is downregulated and positively correlated with prognosis in glioma. Functional experiments showed that overexpression of KB-1460A1.5 inhibits glioma cell proliferation, migration and invasion in vitro and in vivo, while downregulation of KB-1460A1.5 has the opposite effects. Mechanistically, tandem mass tag (TMT)-based quantitative proteomic analysis revealed that KB-1460A1.5 preferentially affects the Akt/TSC1/mTOR pathway. KB-1460A1.5 was found to function as a competing endogenous RNA (ceRNA) to regulate the expression of TSC1, a key regulatory component of the mTOR pathway, by sponging miR-130a-3p in glioma cells. Furthermore, our data demonstrate that the mTOR pathway regulates the expression of the transcription factor Yin Yang 1 (YY1), which in turn binds directly to the KB-1460A1.5 promoter and affects the expression of KB-1460A1.5. Untargeted metabolomics and quantitative real-time PCR (qRT-PCR) analysis further confirmed the effects of KB-1460A1.5 on amino acid metabolism. In conclusion, this study revealed that lncRNA KB-1460A1.5 inhibits glioma tumorigenesis via miR-130a-3p/TSC1/mTOR/YY1 feedback loop.
长链非编码 RNA(lncRNA)与癌症的发生和治疗密切相关。然而,lncRNA 在胶质瘤中的临床意义及其作用机制在很大程度上仍是未知的。在这项研究中,我们使用在线数据集并结合收集的临床胶质瘤组织,确定 lncRNA KB-1460A1.5 在胶质瘤中下调,并与预后呈正相关。功能实验表明,KB-1460A1.5 的过表达抑制了胶质瘤细胞在体外和体内的增殖、迁移和侵袭,而 KB-1460A1.5 的下调则具有相反的效果。从机制上讲,串联质量标签(TMT)-基于定量蛋白质组学分析表明,KB-1460A1.5 优先影响 Akt/TSC1/mTOR 通路。研究发现,KB-1460A1.5 在胶质瘤细胞中作为竞争内源性 RNA(ceRNA)通过海绵吸附 miR-130a-3p 来调节 mTOR 通路的关键调节因子 TSC1 的表达。此外,我们的数据表明 mTOR 通路调节转录因子 Yin Yang 1(YY1)的表达,而 YY1 又直接结合到 KB-1460A1.5 启动子上并影响 KB-1460A1.5 的表达。非靶向代谢组学和定量实时 PCR(qRT-PCR)分析进一步证实了 KB-1460A1.5 对氨基酸代谢的影响。总之,这项研究揭示了 lncRNA KB-1460A1.5 通过 miR-130a-3p/TSC1/mTOR/YY1 反馈环抑制胶质瘤肿瘤发生。