ABSTRACT
OBJECTIVE: The aim of this study was to analyze the role of LINC01554 in the pathogenesis of hepatocellular carcinoma (HCC) and explore the potential mechanism through which LINC01554 affects the migration and proliferation of HCC cells. PATIENTS AND METHODS: LINC01554 expression in HCC tissues and its link to the prognosis of patients were analyzed by The Cancer Genome Atlas (TCGA) database. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to examine LINC01554 levels in 60 cases of HCC clinical tissues and HCC cell lines. Then, LINC01554 overexpression model was constructed using lentivirus in HCC cell lines. HCC proliferation and invasive ability were evaluated through Cell Counting Kit (CCK-8) and transwell tests, respectively. Furthermore, the potential action mechanism of LINC01554 was explored using bioinformatics analysis and in vitro cell experiments. RESULTS: Analysis of the TCGA database revealed that LINC01554 was remarkably under-expressed in HCC tissues. Decreased expression of LINC01554 predicted a poor prognosis for patients. Besides, LINC01554 overexpression markedly blunted the proliferation and migratory capacities of HCC cells. LINC01554 competed with NGFR to bind to microRNA-3681-3p, thereby providing possible mechanisms by which LINC01554 could participate in the progression of HCC. CONCLUSIONS: This study shows for the first time that LINC01554 modulates NGFR expression by binding to microRNA-3681-3p, thereby participating in the progression of HCC.
Subject(s)
Carcinoma, Hepatocellular/metabolism , Liver Neoplasms/metabolism , MicroRNAs/metabolism , Nerve Tissue Proteins/genetics , RNA, Long Noncoding/metabolism , Receptors, Nerve Growth Factor/genetics , Binding Sites , Carcinoma, Hepatocellular/pathology , Cell Movement , Cell Proliferation , Cells, Cultured , Humans , Liver Neoplasms/pathology , MicroRNAs/genetics , Nerve Tissue Proteins/metabolism , RNA, Long Noncoding/genetics , Receptors, Nerve Growth Factor/metabolismABSTRACT
OBJECTIVE: To explore the role of Circular RNA 0091579 in the progression of liver cancer (LCa) and its molecular mechanism. PATIENTS AND METHODS: Quantitative polymerase chain reaction (qPCR) was used to detect circ_0091579 expression levels in LCa tissues and adjacent tissues, which was further verified in LCa cells and normal liver epithelial cells. After circ_0091579 was knocked down in Huh7 and HepG2 cells, cell counting kit-8 (CCK-8), plate cloning and transwell assays were performed to verify the effect of circ_0091579 on cell proliferative ability and metastasis of LCa cells. The starBase database was used to search for microRNAs that could interact with circ_0091579, and the Dual-Luciferase reporter gene was used to verify their binding relationship. RESULTS: circ_0091579 was highly expressed in HCC and HCC cells. In vitro experiments showed that down-regulation of circ_0091579 expression could remarkably inhibit the proliferative ability and metastasis of HCC cells. Bioinformatics software predicted the binding sites between circ_0091579 and microRNA-490-3p, and dual-luciferase reporter gene assay confirmed the binding relationship between circ_0091579 and microRNA-490-3p. qPCR results showed that microRNA-490-3p was remarkably down-regulated in LCa tissues. In vitro experiments confirmed that overexpression of microRNA-490-3p inhibited the proliferative ability and metastasis of HCC cells. CONCLUSIONS: circ_0091579 is abnormally highly expressed in LCa tissues and cells. Down-regulation of circ_0091579 can inhibit the proliferative ability and metastasis of HCC cells by regulating microRNA-490-3p, thus accelerating the progress of the tumor.