中文摘要：

目的：探讨CXCR4特异性非肽类受体拮抗剂AMD3100对胃癌细胞增殖和侵袭能力的影响及其可能的分子机制。方法：Western blot方法检测不同转移潜能胃癌细胞系中CXCR4蛋白的表达水平。以不同浓度的AMD3100处理MKN28-M和MKN28-NM细胞后，采用CCK-8检测胃癌细胞的增殖情况，Transwell实验观察胃癌细胞侵袭能力的变化。Western blot检测AMD3100处理后MKN28-M细胞中基质金属蛋白酶-9（MMP-9）、血管内皮生长因子（VEGF）的表达。结果：Western blot实验结果显示，高转移胃癌细胞MKN28-M中CXCR4的蛋白表达水平明显高于低转移胃癌细胞MKN28-NM，亲本细胞MKN28的CXCR4蛋白表达量很低。CCK-8和 Transwell 实验检测结果表明，AMD3100通过特异性阻断 CXCR4的作用，显著抑制MKN28-M和MKN28-NM细胞的增殖能力（ p〈0.05）和侵袭能力（ p〈0.01），且其抑制均呈剂量依赖性。经AMD3100处理后，MKN28-M细胞中MMP-9和VEGF的蛋白表达水平降低。结论：AMD3100可能通过下调MMP-9、VEGF等分子的表达抑制胃癌细胞的增殖，减弱胃癌细胞的侵袭及转移能力。

英文摘要：

Objective：To explore the effect of AMD3100,which is the specific inhibitor of CXCR4,on proliferation and invasion of gastric cancer cells and its probable mechanism. Methods：Western blot was used to detect the expres-sion of CXC chemokine receptor-4（CXCR4）in different metastatic potential cell lines. AMD3100 at different final concentrations was applied to treat with human gastric cancer cell line MKN28-M and MKN28-NM. CCK-8 assay was used to detect their proliferation. Transwell assay was used to identify the invasive ability in MKN28 -M and MKN28-NM cell lines. Western blot was employed to detect the expressions of matrix metalloproteinase-9（ MMP-9）and vascular endothelial growth factor（VEGF）in MKN28-M cell line after incubation with AMD3100. Results：Western blot showed that expression level of CXCR4 in MKN28-M cells was higher than MKN28-NM,while with hardly expression in MKN28 cells. The proliferation of MKN28-M and MKN28-NM were significantly suppressed by AMD3100 in a dose-dependent manner（p〈0. 05）. AMD3100（100 and 1000ng/ml）significantly inhibited the invasion ability of MKN28-M and MKN28-NM cells（p〈0. 01）. Treatment with AMD3100 markedly reduced the expression of MMP-9 and VEGF in MKN28-M cells . Conclusion：AMD 3 1 0 0 inhibits proliferation and invasion activities of gastric cells may through down-regulation of MMP-9 and VEGF expression.