Long noncoding RNA MSC-AS1 promotes hepatocellular carcinoma oncogenesis via inducing the expression of phosphoglycerate kinase 1

Abstract

Background and Objectives: Increasing studies report that lncRNAs are dysregulated in hepatocellular carcinoma (HCC), which might function as significant diagnostic biomarkers of HCC. LncRNA MSC-AS1 has been newly discovered in several cancers. However, its biological effect in HCC remains to be clearly elucidated. The aim of our work was to test MSC-AS1 expression level and assess its function in HCC progression. Methods: Expression levels of MSC-AS1 and PGK1 in HCC were tested by qRT-PCR in HCC cells including HUH-7, BEL-7404, SNU449, HepG2, QGY-7701, and human normal liver cells (HL-7702 cells). Association of MSC-AS1 expression with various clinicopathological features and patients’ survival were analyzed by chi-squared test and Kaplan-Meier, respectively. The functions of MSC-AS1 in HCC cells were investigated using EdU assay, colony formation, flow cytometry, would healing assay, and Transwell matrigel invasion assays. The correlation between MSC-AS1 and PGK1 was confirmed using a RIP assay. Protein expression of PGK1 was evaluated using a western blot assay. Results: MSC-AS1 was obviously upregulated in HCC tissues and HCC cells. Knockdown of MSC-AS1 repressed HepG2 and BEL-7404 cell proliferation, colony formation capacity, and triggered cell apoptosis. HepG2 and BEL-7404 cell cycle was blocked in G1 phase and cell migration/invasion was remarkably depressed. Downregulation of MSC-AS1 in HCC cells reduced PGK1 expression. In vivo data demonstrated that silence of MSC-AS1 suppressed HCC development via activating PGK1. Conclusions: Taken these together, we indicated that MSC-AS1 promoted HCC oncogenesis via inducing the expression of PGK1.