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作 者:陈惠新[1] 欧志英 陈丽莎[1] 徐永成[1] 曾书君[1] 罗程[1] 余志金[1]
机构地区:[1]惠州市中心人民医院消化内科,广东惠州516001 [2]广州市妇女儿童医疗中心,广东广州510623
出 处:《南京医科大学学报(自然科学版)》2017年第2期184-188,共5页Journal of Nanjing Medical University(Natural Sciences)
基 金:广东省自然科学基金面上项目(S201310011923);惠州市科技计划项目(2013Y009)
摘 要:目的:探讨白介素-8(IL-8)受体促进胃癌侵袭所介导的分子机制。方法:胃癌细胞培养后分别转染空白质粒pc DNA3.1(+)、针对IL-8受体的反义表达质粒pc DNA3.1(+)/as-IL-8G和针对IL-8受体的正义表达质粒pc DNA3.1(+)/s-IL-8G,Western blot检测蛋白表达,细胞侵袭力用相对侵袭细胞数量表示。结果:低表达IL-8受体的胃癌细胞侵袭能力显著减弱,且细胞内c-Jun、Ets-1、MMP-9的蛋白水平显著下降;而高表达IL-8受体的胃癌细胞侵袭能力则显著增强,且细胞内c-Jun、Ets-1、MMP-9的蛋白水平显著上升。用硫代磷酸化修饰的反义寡聚脱氧核苷酸阻断该细胞内c-Jun或Ets-1的表达后,MMP-9的蛋白表达水平显著降低,并伴随细胞侵袭能力明显下降。结论:IL-8受体通过介导c-Jun和Ets-1异常调控MMP-9促进了胃癌细胞的侵袭过程。Objective:To explore the molecular mechanism in which IL-8 receptor promoted gastric cancer metastasis. Methods:Gastric cancer cells were cultured and transfected with IL-8 receptor antisense expression plasmid pc DNA3.1(+)/as-IL-8G and IL-8receptor sense expression plasmid pc DNA3.1(+)/s-IL-8G. Protein expression was detected by Western blotting. Cell invasion was performed in Transwell and the invasion capacity was expressed by the relative invasive cell number. Results:Gastric cancer cells with lower expression of IL-8 receptor had significantly reduced invasion ability,and the expression of c-Jun,Ets-1 and MMP-9decreased correspondingly,while higher expression of IL-8 receptor markedly enhanced the invasion capacity of gastric cancer cells,and the expression of c-Jun,Ets-1 and MMP-9 increased significantly. MMP-9 protein expression level decreased significantly after blocking the c-Jun or Ets-1 expression by phosphorylated modification antisense oligonucleotide technology,and the cell invasion ability decreased obviously at the same time. Conclusion:IL-8 receptor promoted gastric cancer cells metastasis through abnormal cJun and Ets-1-mediated MMP-9.
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