LncRNA AIRN influences the proliferation and apoptosis of hepatocellular carcinoma cells by regulating STAT1 ubiquitination
LncRNA AIRN influences the proliferation and apoptosis of hepatocellular carcinoma cells by regulating STAT1 ubiquitination
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DOI：
10.1007/s12272-021-01317-7
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发表时间：
2021-03-24
影响因子：
6.7
通讯作者：
Zhang, Qiyu
中科院分区：
文献类型：
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作者：
Cai, Huajie;Zheng, Yihu;Zhang, Qiyu
长链非编码RNA（LncRNA）参与了多种人类疾病的发病机制。本研究旨在探讨IGF 2 R非蛋白编码RNA反义核酸（LncRNAAIRN）在肝细胞癌（HCC）发生发展中的作用及其可能机制。使用实时定量聚合酶链反应，我们证实，LncRNA AIRN的表达在肝癌组织和细胞中提高。生物信息学分析表明，LncRNA AIRN和STAT 1之间存在潜在的相互作用，RNA下拉和RNA免疫沉淀证实了这一点。在环己酰亚胺追踪试验中，LncRNA AIRN的敲低增强了STAT 1蛋白的稳定性。在免疫沉淀试验中，LncRNA AIRN的敲低抑制了cullin 4A（CUL 4A）介导的STAT 1蛋白的泛素化。细胞转染、MTT和流式细胞仪分析表明，LncRNA AIRN/STAT 1轴与肝癌细胞增殖和凋亡的调控密切相关。体内实验证实，LncRNA AIRN的敲低抑制HCC的肿瘤生长。我们的数据表明，敲低LncRNA AIRN抑制肝癌细胞增殖，并通过抑制CUL 4A介导的STAT 1蛋白的泛素化促进细胞凋亡。
Long non-coding RNAs (LncRNAs) have been implicated in the pathogenesis of various human diseases. In this study, we probed into the role and potential mechanisms of the antisense of IGF2R non-protein coding RNA (LncRNA AIRN) in the progression of hepatocellular carcinoma (HCC). Using a quantitative real-time polymerase chain reaction, we corroborated that LncRNA AIRN expression was raised in the HCC tissues and cells. The bioinformatic analysis revealed that a potential interaction between LncRNA AIRN and STAT1, which was verified by the RNA pull-down and RNA immunoprecipitation. In the cycloheximide-chase assay, the knockdown of LncRNA AIRN enhanced the stability of STAT1 protein. In the immunoprecipitation assay, the knockdown of LncRNA AIRN restrained the cullin 4A (CUL4A)-mediated ubiquitination of STAT1 protein. The cell transfection, MTT and flow cytometry assays expounded that the LncRNA AIRN/STAT1 axis was bound up with the regulation of the proliferation and apoptosis of HCC cells. The in vivo experiments corroborated that the knockdown of LncRNA AIRN restrained the tumor growth of HCC. Our data expounded that the knockdown of LncRNA AIRN restrained HCC cell proliferation and boosted cell apoptosis by restraining the CUL4A-mediated ubiquitination of STAT1 protein.