| Literature DB >> 31256427 |
Jian-Hong Zhong1,2, Xiao Xiang1,3, Yan-Yan Wang1, Xu Liu1, Lu-Nan Qi1,2, Cheng-Piao Luo4, Wen-E Wei4, Xue-Mei You1,2, Liang Ma1,2, Bang-De Xiang1,2, Le-Qun Li1,2.
Abstract
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.Entities:
Keywords: SNHG16; hepatocellular carcinoma; lncRNA; p62
Year: 2019 PMID: 31256427 DOI: 10.1002/jcp.29023
Source DB: PubMed Journal: J Cell Physiol ISSN: 0021-9541 Impact factor: 6.384