LncRNA SNHG16 aggravates tumorigenesis and development of hepatocellular carcinoma by sponging miR-4500 and targeting STAT3.

Abstract

Hepatocellular carcinoma (HCC) is the most common type of primary liver tumor and becomes a lethal malignancy on account of high mortality and increasing incidence. A growing body of studies has proved that long noncoding RNAs (lncRNAs) participate in the development of diverse cancers. Although it has been commonly accepted that SNHG16 is a procancer gene in numerous cancers, the regulatory mechanism of SNHG16 in HCC still needs more explorations. In this study, our results delineated that SNHG16 presented much higher expression levels in HCC tissues and cells, particularly in advanced stages of HCC. Enhanced SNHG16 expression was strongly related to poor prognosis. SNHG16 facilitated HCC progression by promoting cell proliferation, migration, invasion, and epithelial-mesenchymal transition process as well as inhibiting cell apoptosis. SNHG16 served as a sponge for miR-4500 in HCC and miR-4500 neutralized the influences of SNHG16 knockdown on HCC. SNHG16 was confirmed to compete with signal transducer and activator of transcription 3 (STAT3) to bind with miR-4500. SNHG16 aggravated the development of HCC via sponging miR-4500 so as to upregulate STAT3. In other words, this study was the first to investigate the potential mechanism of SNHG16 in HCC and verified SNHG16 exerted its carcinogenesis by miR-4500/STAT3 axis, suggesting SNHG16 may be a new underlying therapeutic target for HCC treatment.