首页> 中文期刊> 《当代医学科学(英文)》 >Downregulation of LncRNAH19 and MiR-675 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells through AKT/GSK-3β/Cdc25A Signaling Pathway

Downregulation of LncRNAH19 and MiR-675 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells through AKT/GSK-3β/Cdc25A Signaling Pathway

         

摘要

LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma(HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19 siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction(qRT-PCR), and the protein expression of AKT, GSK-3β and Cdc25 A by Western blotting analysis. The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19 siRNA could significantly increase the migration of HCC cells(P<0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19 siRNA could significantly increase the invasion of HCC cells(P<0.01) as compared with the control group. Western blotting analysis showed that the expression levels of AKT and Cdc25 A were significantly increased(P<0.05), and the expression level of GSK-3β was significantly decreased(P<0.05) after treatment with miR-675 inhibitors and LncRNAH19 siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway.

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