The lncRNA SNHG16 affects prognosis in hepatocellular carcinoma by regulating p62 expression

• Published in: Journal of cellular physiology Vol. 235; no. 2; pp. 1090 - 1102
• Main Authors: Zhong, Jian‐Hong, Xiang, Xiao, Wang, Yan‐Yan, Liu, Xu, Qi, Lu‐Nan, Luo, Cheng‐Piao, Wei, Wen‐E, You, Xue‐Mei, Ma, Liang, Xiang, Bang‐De, Li, Le‐Qun
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.02.2020
• Subjects: Apoptosis; Cell migration; Cell proliferation; Diagnostic systems; Hepatocellular carcinoma; Liver cancer; lncRNA; Medical prognosis; Metastases; p62; Prognosis; SNHG16; Survival; Therapeutic applications; TOR protein; Tumors; SNHG16; lncRNA; p62; hepatocellular carcinoma
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.29023

Long noncoding RNAs (lncRNAs) regulate tumor development and progression by promoting proliferation, invasion, and metastasis. The oncogenic role of lncRNA SNHG16 in hepatocellular carcinoma (HCC) has not been revealed. LncRNA SNHG16 is upregulated in HCC and correlates with poorer prognosis. Patients with high SNHG16 expression showed lower rates of overall and disease‐free survival than patients with low SNHG16 expression. Multivariate Cox regression revealed that SNHG16 expression was an independent predictor of poor overall and disease‐free survival. In vitro, SNHG16 promoted HCC cell proliferation, migration, and invasion while inhibiting apoptosis; in vivo, it accelerated tumor development. Altering SNHG16 expression altered levels of miR‐17‐5p, which in turn modified expression of p62, which has been shown to regulate the mTOR and NF‐κB pathways. Indeed, altering SNHG16 expression in HCC cells activated mTOR and NF‐κB signaling. These results reveal a potential mechanism for the oncogenic role of SNHG16 in HCC. SNHG16 may therefore be a promising diagnostic marker as well as therapeutic target in HCC. A schematic hypothetical model shows how SNHG16 acts as an oncogenic long noncoding RNA that promotes hepatocarcinogenesis by acting as a competing endogenous RNA that binds to miR‐17‐5p, thereby de‐repressing expression of p62 and its signal pathways AFB1, aflatoxin B1.