Abstract
Accumulating evidence have suggested that long non-coding RNAs (lncRNAs) had malfunctioning roles in the development of human cancers. The present study aimed to investigate the role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in hepatocellular carcinoma (HCC) progression using human tissues and cell lines. The quantitative real-time PCR results showed that SNHG5 was up-regulated in both HCC tissues and hepatoma cell lines and was closely associated with tumor size, hepatitis B virus infection, histologic grade, TNM stage, and portal vein tumor thrombus (PVTT) in HCC patients. Knockdown of SNHG5 induced apoptosis and repressed cell cycle progression, cell growth, and metastasis in hepatoma cell lines, whereas overexpression of SNHG5 had the opposite effects. In vivo functional assay, xenograft tumors grown from SNHG5-knockdown cells had smaller mean volumes than the tumors grown from negative control cells. Further investigations showed that SNHG5 may act as a competing endogenous RNA by competitively binding miR-26a-5p and thereby modulating the derepression of downstream target GSK3β, which were further confirmed by luciferase reporter assay. Functionally, SNHG5 promotes tumor growth and metastasis by activating Wnt/β-catenin pathway and inducing epithelial to mesenchymal transition (EMT). Taken together, SNHG5 promotes HCC progression by competitively binding miR-26a-5p and regulating GSK3β and Wnt/β-catenin signal pathway.
Highlights
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death worldwide[1]
Results showed that small nucleolar RNA host gene 5 (SNHG5) expression was significantly higher in HCC tissues compared to non-malignant tissues (Fig. 1a)
These results demonstrated that overexpresssion of SNHG5 played a key role in the development and progression of HCC
Summary
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death worldwide[1]. Despite recent advances in the treatment of HCC in surgery, chemotherapy and biologics, it still has a poor prognosis due to tumor metastatic and chemoresistant[2,3]. Tumorigenesis is a complex process involving multiple genetic changes and leading to the malignant transformation[4]. In recent years, emerging evidence suggests that noncoding RNAs (ncRNAs) are involved as important regulators in various physiological and pathological cellular processes[5,6]. Among the large fraction of non-coding transcripts, the class of long non-coding RNAs (lncRNAs), which defined as transcripts longer than 200 nucleotides, is receiving increasing attention and may present new opportunities for disease diagnosis and treatment. In view of tumor biology, dysregulation of lncRNAs could contribute to fundamental aspects of Official journal of the Cell Death Differentiation Association
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