SNHG5 functions as competitive RNA with miR-23c to regulate HMGB2 expression in hepatocellular carcinoma.

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. In vitro 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. AJTR