Silence of long non-coding RNA KCNQ1OT1 inhibits the proliferation, migration and invasion of hepatocellular carcinoma cells through PI3K/AKT signaling pathway

Abstract

Background: KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) has been reported to be associated with hepatocellular carcinoma (HCC), which is considered as one of the most common cancers worldwide. However, the mechanism of action of KCNQ1OT1 in human HCC has not been fully explained. In this study, we aimed to explore the functional role and the potential mechanism of KCNQ1OT1 in human HCC.Methods: First, we analyzed the expression levels of KCNQ1OT1 in HCC tissues in starBase database and detected the expression of KCNQ1OT1 in HCC cell lines by quantitative real-time polymerase chain reaction assays. Next, we analyzed the role of KCNQ1OT1 in migration, invasion and proliferation of HCC by scratch wound healing, transwell and cell counting kit-8 assays. Finally, we analyzed the potential interrelationship between KCNQ1OT1 and PI3K/AKT signaling pathway through western blot assays.Results: Based on bioinformatics analyses, we found that KCNQ1OT1 was highly expressed in HCC tissues and its high expression was associated with a poor prognosis in HCC patients. We also confirmed an abnormal increase in the expression of KCNQ1OT1 in HCC cell lines. KCNQ1OT1 knockdown was found to have a negative impact on proliferation, migration and invasion of HCC cells. In addition, interference with the expression of KCNQ1OT1 reduced the phosphorylation level of AKT and the protein level of PI3K, indicating the association of KCNQ1OT1 with the PI3K/AKT signaling pathway.Conclusions: Collectively, this study confirmed the important role of KCNQ1OT1 in promoting HCC growth and revealed the inhibitory effect of KCNQ1OT1 on the PI3K/AKT signaling pathway. This work may contribute to a better understanding of HCC progression and provide a potential biomarker for HCC.