IL-8受体介导c-Jun和Ets-1异常调控MMP-9促进胃癌细胞侵袭

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pcDNA3.1(+)?针对IL-8受体的反义表达质粒pcDNA3.1(+)/as-IL-8G和针对IL-8受体的正义表达质粒pcDNA3.1(+)/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?

IL-8 receptor mediated c-Jun and Ets-1 abnormal promoted gastric cancer cells metastasis through MMP-9

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 pcDNA3.1(+)/as-IL-8G and IL-8 receptor sense expression plasmid pcDNA3.1(+)/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-9 decreased 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 c-Jun and Ets-1-mediated MMP-9.