Small nucleolar RNA host gene 3 functions as a novel biomarker in liver cancer and other tumour progression

Abstract

Cancer has become the most life-threatening disease in the world. Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs, especially long noncoding RNAs (lncRNAs), have significant effects in human cancers. LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes. Small nucleolar RNA host gene 3 (SNHG3) is a novel lncRNA and has been reported to be differentially expressed in various tumors, such as liver cancer, gastric cancer, and glioma. However, the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood. In this review, we summarize the results of SNHG3 studies in humans, animal models, and cells to underline the expression and role of SNHG3 in cancer. SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis. SNHG3 expression in lung adenocarcinoma remains controversial. Concurrently, SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms, including competing endogenous RNA effects. A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.

Keywords: Small nucleolar RNA host gene 3; Long noncoding RNAs, Biomarker; Clinical characters; Molecular mechanism; Competing endogenous RNA; Liver cancer

Core Tip: This review explores the differential expression of small nucleolar RNA host gene 3 (SNHG3) as a novel lncRNA in hepatocellular carcinoma as well as other tumours. SNHG3 is upregulated in most tumours and can influence tumourigenesis and progression through competing endogenous RNA effects and signalling pathways, thereby adversely affecting patient prognosis. Therefore, SNHG3 may become a new target for the diagnosis and treatment of many cancers, including hepatocellular carcinoma.