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CCL22-CCR4轴在胃癌腹膜乳斑转移的机制研究
引用本文:黄罡,胡祥,曹亮,罗红.CCL22-CCR4轴在胃癌腹膜乳斑转移的机制研究[J].中华普通外科杂志,2010,25(4).
作者姓名:黄罡  胡祥  曹亮  罗红
作者单位:1. 大连医科大学附属第一医院普外科,辽宁省,116011
2. 大连医科大学免疫微生物检验教研室
摘    要:目的 探讨巨噬细胞衍生因子MDC/CCL22-CCR4反应轴在胃癌腹膜乳斑转移中的作用.方法 用RT-PCR和Western blot方法检测CCR4在5种胃癌细胞系中的表达;MTT法测定不同浓度CCL22对胃癌细胞株BGC-823增殖率的变化;Transwell小室体外侵袭实验检测CCL22对胃癌细胞株BGC-823趋化活性的影响;免疫组化检测标本中CCR4表达;单变量分析CCR4表达与胃癌临床病理参数的关系.结果 CCR4mRNA和CCR4蛋白在5种胃癌细胞系中均有表达.CCL22可以促进BGC-823细胞的增殖和趋化.CCR4在胃癌中有表达,CCR4表达水平与胃癌分化程度相关(P<0.05),而与患者的年龄、肿瘤大小、位置、分期以及淋巴结转移等均无关(P>0.05).结论 CCL22-CCR4反应轴可能在胃癌腹膜乳斑转移中起作用.CCR4可能成为预防和治疗胃癌腹膜转移的潜在靶点.

关 键 词:胃肿瘤  肿瘤转移  趋化因子  巨噬细胞  乳斑

MDC/CCL22-CCR4 axis in milky spots in peritoneal carcinomatosis of gastric cancer
HUANG Gnng,HU Xiang,CAO Liang,LUO Hong.MDC/CCL22-CCR4 axis in milky spots in peritoneal carcinomatosis of gastric cancer[J].Chinese Journal of General Surgery,2010,25(4).
Authors:HUANG Gnng  HU Xiang  CAO Liang  LUO Hong
Abstract:Objective To study the role of MDC/CCL22-CCR4 axis in milky spots in peritoneal carcinomatosis of gastric cancer.Methods We examined the expression of CCR4 in 5 gastric cancer cell lines by RT-PCR and Western-blot.Cell growth rate of BGC-823 cell lines before and after incubated with CCL22 was detemined by MTT assay.The effects of CCL22 on invasion of BGC-823 cells into Matrigel were measured using Transwell test.Immunohistochemistry was conducted to detect the expression of CCR4.Results CCR4 mRNA and protein expression were detected in all 5 human gastric cancer cell lines:CCL22had a direct promotive effect on BGC-823 cell prolifetation and invasion.There was CCR4 expression in Stomach neoplasms.The expression of CCR4 in primary tumor was correlated with tumor pathological differentiation(P<0.05),but not with age of patients,gender,location of tumor,tumor size,tumor stage,lymph node metastasis(P>0.05).Conclusions The MDC/CCL22-CCR4 axis may be one of the mechanism of peritoneal metastasis in milky spot in gastric cancer.
Keywords:Stomach neoplasms  Neoplasm metastasis  Chemotactic factors  macrophage  Milky spot
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