LncRNA SNHG17 Contributes to Proliferation, Migration, and Poor Prognosis of Hepatocellular Carcinoma. (14th September 2021)

• Record Type: Journal Article
• Authors: Luo, Yue; Lin, Junhao; Zhang, Jiakang; Song, Zhenghui; Zheng, Dayong; Chen, Fengsheng; Zhuang, Xuefen; Li, Aimin; Liu, Xinhui
• Other Names: Solimando Antonio Giovanni Academic Editor.
• Is Part Of: Canadian journal of gastroenterology & hepatology. Volume 2021(2021)
• Publication Date: 2021-09-14
• Subjects: Digestive organs -- Diseases -- Periodicals; Gastroenterology -- Periodicals; Digestive organs -- Diseases; Gastroenterology; Canada; Digestive System Diseases -- Periodicals; Gastroenterology -- Periodicals; Periodicals; Electronic journals; Fulltext; Internet Resources; Periodicals; 616.3
• DOI: 10.1155/2021/9990338
• Languages: English
• ISSNs: 2291-2789

Abstract

Abstract : Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis in recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclear. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent nontumorous tissues, and cell lines. The effect of SNHG17 on proliferation, migration, and apoptosis of HCC was investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation, and apoptotic pathway; among them, 92 were overlapped with SNHG17-related genes in the TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2, and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.