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过表达KLF17对结直肠癌细胞SW480血管生成拟态以及体外侵袭能力的影响 被引量:3

Effects of KLF17 overexpression on the vasculogenic mimicry and the invasion of colorectal carcinoma SW480 cells
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摘要 目的:探讨转染KLF17基因对人结直肠癌血管生成拟态及体外侵袭能力的影响。方法:将KLF17表达质粒PIRES-EGFP-KLF17转染至SW480细胞中,以未转染质粒的细胞作为对照;荧光定量PCR和Western blotting法检测转染前后KLF17和血管生成拟态相关基因血管上皮钙黏附素(VE-cadherin)、基质金属蛋白酶-2(MMP-2)和粘连蛋白5γ2链(LN-5γ2)的mRNA和蛋白表达水平; Transwell实验检测KLF17基因转染对SW480细胞体外侵袭能力的影响。结果:转染KLF17表达质粒后SW480细胞中的KLF17基因和蛋白表达水平均显著高于正常细胞(P <0. 01)。过表达KLF17后SW480细胞中VE-cadherin、MMP-2和LN-5γ2的表达量以及细胞侵袭能力显著降低。结论:转染KLF17可以抑制结直肠癌细胞血管生成拟态相关基因的表达,抑制其血管拟态的形成,降低其体外侵袭能力。 Objective:To investigate the effect of KLF17 on the vasculogenic mimicry and invasion of colorectal carcinoma cells.Methods:The recombination KLF17 expression plasmid with EGFP was transfected into SW480 cells,cells without transfected plasmid as the control group.The changes of vasculogenic mimicry associated genes VE-cadherin,MMP-2 and LN-5γ2 in SW480 cells were detected by real-time PCR and Western blotting after KLF17 transfection.Transwell was used to investigate the effects of KLF17 gene on the invasive potential of SW480 cells.Results:KLF17 expression level in overexpression KLF17 group was higher than that of control group(P<0.01).After transfection,the expression levels of VE-cadherin,MMP-2 and LN-5γ2 were down-regulated in SW480 cells.The invasive of SW480 cells was remarkably inhibited by KLF17 transfection.Conclusion:KLF17 gene may inhibit the invasion and prevent the development of vasculogenic mimicry by down-regulating the related genes expression in colorectal carcinoma.
作者 陈华涛 瞿紫微 孟庆彬 肖新波 赵春翔 CHEN Huatao;QU Ziwei;MENG Qingbin;XIAO Xinbo;ZHAO Chunxiang(Department of Gastrointestinal Surgery,the First Hospital of Wuhan,Wuhan 430022,China)
出处 《东南大学学报(医学版)》 CAS 2018年第5期760-764,共5页 Journal of Southeast University(Medical Science Edition)
基金 湖北省卫生计生委科研基金资助项目(WJ2015Z063) 武汉市卫生计生委科研基金资助项目(WX16C39) 湖北省自然科学基金一般面上项目(2016CFB595)
关键词 血管生成拟态 结直肠癌 KLF17 VE-CADHERIN MMP-2 LN-5γ2 vasculogenic mimcry colorectal carcinoma KLF 17 VE-cadherin MMP-2 LN-5γ2
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