PURPOSE: Hepatocellular carcinoma (HCC) is one of the common cancers, but its relationship with long non-coding (lnc)RNA XIST and microRNA (miR)-488 is still under investigation. Therefore, this study aimed to explore the correlation between miR-488 and XIST in HCC. METHODS: qRT-PCR was employed to quantify the lncRNA XIST and miR-488 in HCC tissues and cells, and miR-488 mimcs and lncRNA siRNA vectors were constructed for analysis of the roles of miR-488 and lncRNA XIST in HCC cells. Flow cytometry was applied to determine the cell cycle and apoptosis, Western blot assay to detect apoptosis-related proteins, and the MTT assay to detect cell viability. RESULTS: lncRNA XIST was highly expressed in HCC, while miR-488 was lowly expressed. Silencing lncRNA XIST gave rise to an increase in G0/G1 phase cells and a decrease in S-phase cells, promoted apoptosis, weakened cell viability, and induced up-regulation of Caspase-3, Caspase-9, and Bax, and up-regulating miR-488 led to similar results. The dual luciferase reporter gene assay confirmed that lncRNA XIST could bind to miR-488, and its inhibition could give rise to up-regulation of miR-488. It was also confirmed that lncRNA XIST was negatively correlated with miR-488. CONCLUSION: LncRNA XIST accelerates HCC cell growth by inhibiting miR-488, so inhibiting lncRNA XIST or up-regulating miR-488 has objective potential therapeutic value and may be helpful for the development of new HCC treatment strategies.
PURPOSE:Hepatocellular carcinoma (HCC) is one of the common cancers, but its relationship with long non-coding (lnc)RNA XIST and microRNA (miR)-488 is still under investigation. Therefore, this study aimed to explore the correlation between miR-488 and XIST in HCC. METHODS: qRT-PCR was employed to quantify the lncRNA XIST and miR-488 in HCC tissues and cells, and miR-488 mimcs and lncRNA siRNA vectors were constructed for analysis of the roles of miR-488 and lncRNA XIST in HCC cells. Flow cytometry was applied to determine the cell cycle and apoptosis, Western blot assay to detect apoptosis-related proteins, and the MTT assay to detect cell viability. RESULTS: lncRNA XIST was highly expressed in HCC, while miR-488 was lowly expressed. Silencing lncRNA XIST gave rise to an increase in G0/G1 phase cells and a decrease in S-phase cells, promoted apoptosis, weakened cell viability, and induced up-regulation of Caspase-3, Caspase-9, and Bax, and up-regulating miR-488 led to similar results. The dual luciferase reporter gene assay confirmed that lncRNA XIST could bind to miR-488, and its inhibition could give rise to up-regulation of miR-488. It was also confirmed that lncRNA XIST was negatively correlated with miR-488. CONCLUSION: LncRNA XIST accelerates HCC cell growth by inhibiting miR-488, so inhibiting lncRNA XIST or up-regulating miR-488 has objective potential therapeutic value and may be helpful for the development of new HCC treatment strategies.