LncRNA AIRN infl uences the proliferation and apoptosis of hepatocellular carcinoma cells by regulating STAT1 ubiquitination

• Published in: Archives of pharmacal research pp. 414 - 426
• Main Authors: Huajie Cai, Yihu Zheng, Zhengde Wen, Yingnan Yang, Shouzhang Yang, Qiyu Zhang
• Format: Journal Article
• Language: English
• Published: 대한약학회 01.04.2021
• Subjects: 약학
• ISSN: 0253-6269; 1976-3786
• DOI: 10.1007/s12272-021-01317-7

Long non-coding RNAs (LncRNAs) havebeen implicated in the pathogenesis of various human diseases. In this study, we probed into the role and potentialmechanisms of the antisense of IGF2R non-protein codingRNA (LncRNA AIRN) in the progression of hepatocellularcarcinoma (HCC). Using a quantitative real-timepolymerase chain reaction, we corroborated that LncRNAAIRN expression was raised in the HCC tissues and cells. The bioinformatic analysis revealed that a potential interactionbetween LncRNA AIRN and STAT1, which wasverifi ed by the RNA pull-down and RNA immunoprecipitation. In the cycloheximide-chase assay, the knockdown ofLncRNA AIRN enhanced the stability of STAT1 protein. Inthe immunoprecipitation assay, the knockdown of LncRNAAIRN restrained the cullin 4A (CUL4A)-mediated ubiquitinationof STAT1 protein. The cell transfection, MTT andfl ow cytometry assays expounded that the LncRNA AIRN/STAT1 axis was bound up with the regulation of the proliferationand apoptosis of HCC cells. The in vivo experimentscorroborated that the knockdown of LncRNA AIRNrestrained the tumor growth of HCC. Our data expoundedthat the knockdown of LncRNA AIRN restrained HCC cellproliferation and boosted cell apoptosis by restraining theCUL4A-mediated ubiquitination of STAT1 protein. KCI Citation Count: 3