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首页> 外文期刊>Cancer Management and Research >lncRNA TUG1 Promotes Cell Proliferation, Migration, and Invasion in Hepatocellular Carcinoma via Regulating miR-29c-3p/ COL1A1 Axis
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lncRNA TUG1 Promotes Cell Proliferation, Migration, and Invasion in Hepatocellular Carcinoma via Regulating miR-29c-3p/ COL1A1 Axis

机译:LNCRNA Tug1通过调节miR-29c-3p / col1a1轴来促进肝细胞癌中的细胞增殖,迁移和侵袭

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Background: Taurine upregulated gene 1 (TUG1) has been recognized as a novel oncogenic gene. The current study was established to explore the function and regulatory mechanism of TUG1 in hepatocellular carcinoma (HCC). Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of TUG1, miR-29c-3p, and COL1A1 in tissues and cell lines. MTT assay, wound-healing and transwell assay were utilized for the detection of cell viability, migration and invasion, respectively. The interactions between miR-29c-3p and TUG1/ COL1A1 were predicted by starBase v2.0 ( http://starbase.sysu.edu.cn/ ) and verified by the dual-luciferase reporter or RNA immunoprecipitation assay. Western blot assay was performed to determine the protein levels of COL1A1, cyclin D1, E-cadherin, N-cadherin, Bcl-2, and Bax. Results: Dramatically increased expression of TUG1 was noticed in HCC tissues and cell lines. TUG1 knockdown restrained the proliferation, migration, and invasion, and promoted the apoptosis of HCC cells. TUG1 targeted miR-29c-3p and inhibited miR-29c-3p expression. Overexpression of miR-29c-3p inhibited the proliferation, migration and invasion of HCC cells. MiR-29c-3p directly targeted COL1A1 and down-regulated COL1A1 expression. In addition, downregulation of miR-29c-3p and upregulation of COL1A1 both reversed the effects of TUG1 knockdown on the proliferation, apoptosis, migration, and invasion of HCC cells. Conclusion: TUG1 could promote the proliferation, migration and invasion of HCC cells through regulating miR-29c-3p/ COL1A1 axis. This novel finding might provide a latent target for the treatment of HCC.
机译:背景:牛磺酸上调基因1(Tug1)被认为是一种新的致癌基因。建立了目前的研究,以探讨Tug1在肝细胞癌(HCC)中的功能和调节机制。方法:使用定量实时聚合酶链反应(QRT-PCR)检测Tug1,miR-29c-3p和Col1a1在组织和细胞系中的表达。 MTT测定,伤口愈合和Transwell测定分别用于检测细胞活力,迁移和侵袭。 MiR-29C-3P和Tug1 / COL1A1之间的相互作用由Starbase V2.0(http://starbase.sysu.edu.cn/)预测并由双荧光素酶报告器或RNA免疫沉淀测定验证。进行蛋白质印迹测定以确定COL1A1,细胞周期蛋白D1,E-CDADHERIN,N-CADERIN,BCL-2和BAX的蛋白质水平。结果:在HCC组织和细胞系中,注意到Tug1的表达显着增加。 Tug1敲低抑制了增殖,迁移和侵袭,并促进了HCC细胞的凋亡。 Tug1靶向miR-29c-3p并抑制miR-29c-3p表达。 miR-29c-3p的过表达抑制了HCC细胞的增殖,迁移和侵袭。 miR-29c-3p直接针对col1a1和下调的col1a1表达。此外,MIR-29C-3P的下调和COL1A1的上调均逆转Tug1敲低对HCC细胞增殖,凋亡,迁移和侵袭的影响。结论:Tug1可以通过调节miR-29c-3p / col1a1轴来促进HCC细胞的增殖,迁移和侵袭。这部小说发现可能为治疗HCC提供潜在目标。

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