Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression

• Main Authors: Jidong Sui, Xuejun Yang, Wenjing Qi, Kun Guo, Zhenming Gao, Liming Wang, Deguang Sun
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2017-11-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Long non-coding RNA; PTEN; miR-21; AKT; Hepatocellular Carcinoma
• Online Access: https://www.karger.com/Article/FullText/485449

Background/Aims: Recent evidence has indicated the crucial regulatory roles of long non-coding RNAs (lncRNAs) in tumour biology. In hepatocellular carcinoma (HCC), aberrant expression of lncRNAs plays an essential role in HCC tumourigenesis. However, the potential roles and regulatory mechanisms of the novel human lncRNA, Linc-USP16, in HCC are unclear. Methods: To investigate the function of Linc-USP16 in HCC, we first analysed the expression levels of Linc-USP16 in HCC patient tissues and cell lines via q-RT-PCR and established overexpressed or knockdown HCC cell lines. Results: Here, we found that Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p. These interactions led to repression of AKT pathway and inhibition of HCC cell proliferation and migration. Conclusion: Thus, our data showed that Linc-USP16, as a tumour suppressor, plays an important role in HCC pathogenesis and provides a new therapeutic strategy for HCC treatment.