Li Wenchuan, Lu Yuan, Wu Yi, Qin Zebang, Tang Qianli, Wei Huamei, Wang Jianchu, Pu Jian
Department of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities Guangxi, China.
Graduate College, Youjiang Medical University for Nationalities Guangxi, China.
Am J Transl Res. 2020 May 15;12(5):2192-2200. eCollection 2020.
Emerging evidence demonstrated long non-coding RNA (lncRNA) small nucleolar RNA host gene 5 (SNHG5) participates in the tumorigenesis. The aim of this work was to characterize the expression and biology roles of SNHG5 in hepatocellular carcinoma (HCC). Expression level of SNHG5 in HCC cells was analyzed with RT-qPCR. Cell proliferation rate, cell cycle distribution, and cell migration ability was analyzed with cell counting kit-8 assay, flow cytometry, and wound-healing assay, respectively. Targets prediction were performed at LncBase V2.0 and TargetScan. SNHG5 was found elevated expression in HCC cell lines. functional experiments showed knockdown of SNHG5 inhibits cell proliferation and migration, while overexpression of SNHG5 exerted opposite effects. Mechanism studies showed SNHG5 functions as competitive endogenous RNA (ceRNA) for microRNA-23c (miR-23c) to promote high mobility group box 2 (HMGB2) expression. miR-23c was downregulated, while HMGB2 was upregulated in HCC tissues and cells. We revealed SNHG5 could exert an oncogenic role in HCC via regulating miR-23c/HMGB2 axis. Targeting SNHG5 might be a novel therapeutic measure to suppresses HCC progression.
新出现的证据表明，长链非编码RNA（lncRNA）小核仁RNA宿主基因5（SNHG5）参与肿瘤发生。本研究旨在表征SNHG5在肝细胞癌（HCC）中的表达及生物学作用。采用RT-qPCR分析HCC细胞中SNHG5的表达水平。分别采用细胞计数试剂盒-8法、流式细胞术和伤口愈合试验分析细胞增殖率、细胞周期分布和细胞迁移能力。在LncBase V2.0和TargetScan上进行靶标预测。发现SNHG5在HCC细胞系中表达升高。功能实验表明，敲低SNHG5可抑制细胞增殖和迁移，而SNHG5的过表达则产生相反的效果。机制研究表明，SNHG5作为微小RNA-23c（miR-23c）的竞争性内源性RNA（ceRNA），促进高迁移率族蛋白B2（HMGB2）的表达。在HCC组织和细胞中，miR-23c表达下调，而HMGB2表达上调。我们揭示了SNHG5可能通过调节miR-23c/HMGB2轴在HCC中发挥致癌作用。靶向SNHG5可能是抑制HCC进展的一种新的治疗措施。
