CAJ | 학술논문

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。
목적：탐토CXCR4특이성비태류수체길항제AMD3100대위암세포증식화침습능력적영향급기가능적분자궤제。방법：Western blot방법검측불동전이잠능위암세포계중CXCR4단백적표체수평。이불동농도적AMD3100처리MKN28-M화MKN28-NM세포후，채용CCK-8검측위암세포적증식정황，Transwell실험관찰위암세포침습능력적변화。Western blot검측AMD3100처리후MKN28-M세포중기질금속단백매-9（MMP-9）、혈관내피생장인자（VEGF）적표체。결과：Western blot실험결과현시，고전이위암세포MKN28-M중CXCR4적단백표체수평명현고우저전이위암세포MKN28-NM，친본세포MKN28적CXCR4단백표체량흔저。CCK-8화 Transwell 실험검측결과표명，AMD3100통과특이성조단 CXCR4적작용，현저억제MKN28-M화MKN28-NM세포적증식능력（ p<0.05）화침습능력（ p<0.01），차기억제균정제량의뢰성。경AMD3100처리후，MKN28-M세포중MMP-9화VEGF적단백표체수평강저。결론：AMD3100가능통과하조MMP-9、VEGF등분자적표체억제위암세포적증식，감약위암세포적침습급전이능력。
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.