Wei Li1, Jinzhao Ge2, Jinju Xie1, Jidong Yang1, Jin'e Chen1, Tao He3. 1. Department of Vascular Intervention, Jingmen No.2 People's Hospital, Jingmen, China. 2. Department of Interventional Medicine, Zaozhuang Municipal Hospital, Zaozhuang, China. 3. Department of Interventional Medicine, The Second People's Hospital of Huaihua, Huaihua, China.
Abstract
Background: The current study aimed to investigate the effects of TUG1 on the migration and invasion of hepatoma cells. Materials and Methods: The expressions of TUG1, miR-137, and AKT2 were detected in hepatoma tissues and cells by performing quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The correlations among TUG1, miR-137, and AKT2 were predicted by bioinformatics analysis and confirmed by dual-luciferase reporter assay, and Pearson test was performed to analyze their relevance. The effects of TUG1, miR-137, and AKT2 on viability, migration, and invasion of transfected hepatoma cells were detected by CCK-8, wound scratch, and Transwell. Epithelial-mesenchymal transition (EMT)-related protein levels were determined by Western blot and qRT-PCR. Results: TUG1 was highly expressed in hepatoma tissues and cells. Silencing TUG1 expression inhibited the viability, migration, and invasion of hepatoma cells. TUG1 targeted miR-137 and the two was negatively correlated, and silencing TUG1 expression inhibited the effects of low-expressed miR-137 on promoting proliferation, migration, and invasion of hepatoma cells. AKT2 was predicted to be the target gene for miR-137, and the two were negatively correlated. Moreover, inhibiting miR-137 expression promoted the expression of MMP2, MMP9, and N-cadherin and inhibited E-cadherin expression, while silencing TUG1 expression reversed the effects of low-expressed miR-137 on EMT-related protein levels. Conclusion: LncRNA TUG1 promotes hepatocellular carcinoma migration and invasion through targeting the miR-137/AKT2 axis.
Background: The current study aimed to investigate the effects of TUG1 on the migration and invasion of hepatoma cells. Materials and Methods: The expressions of TUG1, miR-137, and AKT2 were detected in hepatoma tissues and cells by performing quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The correlations among TUG1, miR-137, and AKT2 were predicted by bioinformatics analysis and confirmed by dual-luciferase reporter assay, and Pearson test was performed to analyze their relevance. The effects of TUG1, miR-137, and AKT2 on viability, migration, and invasion of transfected hepatoma cells were detected by CCK-8, wound scratch, and Transwell. Epithelial-mesenchymal transition (EMT)-related protein levels were determined by Western blot and qRT-PCR. Results: TUG1 was highly expressed in hepatoma tissues and cells. Silencing TUG1 expression inhibited the viability, migration, and invasion of hepatoma cells. TUG1 targeted miR-137 and the two was negatively correlated, and silencing TUG1 expression inhibited the effects of low-expressed miR-137 on promoting proliferation, migration, and invasion of hepatoma cells. AKT2 was predicted to be the target gene for miR-137, and the two were negatively correlated. Moreover, inhibiting miR-137 expression promoted the expression of MMP2, MMP9, and N-cadherin and inhibited E-cadherin expression, while silencing TUG1 expression reversed the effects of low-expressed miR-137 on EMT-related protein levels. Conclusion: LncRNA TUG1 promotes hepatocellular carcinoma migration and invasion through targeting the miR-137/AKT2 axis.