LncRNA SNHG3, a potential oncogene in human cancers

Abstract

Long noncoding RNAs (lncRNAs) are composed of > 200 nucleotides; they lack the ability to encode proteins but play important roles in a variety of human tumors. A large number of studies have shown that dysregulated expression of lncRNAs is related to tumor oncogenesis and progression. Emerging evidence shows that SNHG3 is a novel oncogenic lncRNA that is abnormally expressed in various tumors, including osteosarcoma, liver cancer, lung cancer, etc. SNHG3 primarily competes as a competitive endogenous RNA (ceRNA) that targets tumor suppressor microRNAs (miRNAs) and ceRNA mechanisms that regulate biological processes of tumors. In addition, abnormal expression of SNHG3 is significantly correlated with patient clinical features. Upregulation of SNHG3 contributes to biological functions, including tumor cell proliferation, migration, invasion and EMT. Therefore, SNHG3 may represent a potential diagnostic and prognostic biomarker, as well as a novel therapeutic target.

Keywords: Biomarker; Cancer; LncRNA; SNHG3.

Fig. 1

The regulatory molecular mechanisms of SNHG3 in tumorigenesis and progression. Nuclear: (1) DNA methylation is affected by the regulation of methylase. (2) Interaction with transcription factors and suppression of gene transcription. Cytoplasm: (3) MiRNA sponging and miRNA target release. (4) Inhibition of translation

Fig. 2

SNHG3 as a competing endogenous RNA (ceRNA) in a variety of cancers. SNHG3 regulates the expression of mRNAs by competitively binding microRNAs, such as miR-384, miR-330-5p, miR-326, miR-151a-3p, miR-196a-3p, miR-384, miR-340-5p, miR-182-5p, miR-539, miR-139-5p, miR-326, miR-128, miR-758-3p, miR-577, miR-515-5p, and miR-214-3p, which control cell proliferation, apoptosis, migration, invasion, EMT, cell cycle arrest, cell viability and therapeutic resistance