论文部分内容阅读
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 investigate the molecular mechanism mediated by interleukin-8 (IL-8) receptor in gastric cancer invasion. Methods: The gastric cancer cells were transfected with pcDNA3.1 (+), pcDNA3.1 (+) / as-IL-8G antisense plasmid and IL-8 receptor Of the positive expression plasmid pcDNA3.1 (+) / s-IL-8G, Western blot detection of protein expression, cell invasion was expressed as the number of relative invasion of cells. Results: The invasiveness of gastric cancer cells with low expression of IL-8 receptor was significantly decreased, and the protein levels of c-Jun, Ets-1 and MMP-9 were significantly decreased. However, the invasion ability of gastric cancer cells with high expression of IL-8 receptor Was significantly increased, and intracellular c-Jun, Ets-1, MMP-9 protein levels increased significantly. After the expression of c-Jun or Ets-1 was blocked by the phosphorothioated antisense oligodeoxynucleotide, the protein expression of MMP-9 was significantly decreased, accompanied by a significant decrease of cell invasion. Conclusion: IL-8 receptor can promote the invasion of gastric cancer cells by mediating the abnormal regulation of MMP-9 by c-Jun and Ets-1.