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.

Long non-coding RNA MSC-AS1 facilitates the proliferation and glycolysis of gastric cancer cells by regulating PFKFB3 expression

“…Compared to carcinoembryonic antigen, the exosomal lncUEGC1 in the serum shows a higher diagnostic accuracy for discriminating GC patients from healthy individuals [28]. The expression of MSC-AS1 is frequently overexpressed in PDAC, HCC, RCC, and NPC [18][19][20][21]. Moreover, the high level of MSC-AS1 predicts poor clinical outcomes of patients with PDAC, HCC, and RCC [18,19,21].…”

“…Previous studies have explored the biological function of MSC-AS1 in human cancers, including PDAC, HCC, RCC, and NPC [18][19][20][21]. MSC-AS1 knockdown induces proliferation inhibition, apoptosis, and G1 phase arrest, and represses cell migration/invasion in HCC cells [19]. MSC-AS1 participates in tumor progression via promoting cell proliferation and invasion in NPC and RCC [18,20].…”

“…The expression of MSC-AS1 is frequently overexpressed in PDAC, HCC, RCC, and NPC 18 - 21 . Moreover, the high level of MSC-AS1 predicts poor clinical outcomes of patients with PDAC, HCC, and RCC 18 , 19 , 21 . Here, we revealed an upregulated expression of MSC-AS1 in GC tissues and cells.…”

“…Besides, lncRNA MACC1-AS1 enhances GC cells' proliferation and glycolysis via the AMPK/Lin28 pathway-mediated MACC1 upregulation 17 . LncRNA musculin antisense RNA 1 (MSC-AS1) has been recognized as an oncogene in pancreatic ductal adenocarcinoma (PDAC) 18 , hepatocellular carcinoma (HCC) 19 , nasopharyngeal carcinoma (NPC) 20 , and renal cell carcinoma (RCC) 21 . MSC-AS1 functions as a molecular sponge for miR-29b-3p to increase cyclin-dependent kinase 14 (CDK14) expression, which facilitates PDAC cell proliferation 18 .…”

“…MSC-AS1 is reported to promote the proliferation, apoptosis resistance, invasion, and epithelial-to-mesenchymal transition (EMT) of NPC cells by regulating the miR-524-5p/nuclear receptor subfamily 4 group A member 2 (NR4A2) axis 20 . Moreover, MSC-AS1 accelerates HCC progression through enhancing the expression of phosphoglycerate kinase 1 19 . However, it is unclear whether and how MSC-AS1 participates in GC progression.…”