目的：探讨单核细胞趋化蛋白-1(monocyte chemoatractant protein-1, MCP-1)/趋化因子（C-C模体）受体2\[chemokine (C-C motif) receptor 2, CCR2)轴在人脐带间充质干细胞（human umbilical cord mesenchymal stem cells, HUMSCs）向肺癌归巢中的作用。方法：采用组织块培养法从健康新生儿脐带组织中分离HUMSCs并鉴定，构建BALB/c裸鼠皮下移植瘤模型。体外应用Transwell趋化实验、体内应用IVIS Xenogen动物活体成像系统检测HUMSCs是否向肺癌归巢，ELISA法检测肺癌细胞A549培养上清中MCP-1分泌水平，转染shRNA敲低肺癌细胞内MCP-1的表达和用抑制剂RS504393抑制HUMSCs细胞表面的MCP-1受体CCR2后，体内外检测HUMSCs向肺癌归巢能力的改变。结果：成功分离得到HUMSCs并完成鉴定，成功建立BALB/c裸鼠皮下肺癌移植瘤模型。HUMSCs在体内外均能向肺癌归巢（P<0.01），肺癌细胞高表达MCP-1。成功构建稳定低表达MCP-1的肺癌A549细胞系，与对照组相比，shRNA1和shRNA2敲低组趋化HUMSCs的数目明显减少\[（80.0±33.0）、（94.0±16.0） vs （167.0±41.0）个，均P<0.05\]，抑制HUMSCs细胞表面MCP-1受体CCR2后，体内外均显著抑制HUMSCs向肺癌的趋化能力（P<0.05）。结论： MCP-1/CCR2轴促进HUMSCs向肺癌归巢

Objective:To study the role of monocyte chemoatractant protein-1 (MCP-1)/(chemokine \[C-C motif\] receptor 2, CCR2) axis in human umbilical cord mesenchymal stem cells（HUMSCs） homing to lung cancer. Methods: “Tissue explant” method was used to isolate and identify HUMSCs from umbilical cord of healthy newborns. Subcutaneous lung cancer xenograft model was established in nude BALB/c mice. Transwell migration assay in vitro and IVIS Xenogen living imaging system in vivo were applied respectively to investigate the capability of HUMSCs homing to lung cancer. ELISA was utilized to detect the secretion of monocyte chemoatrractant protein-1（MCP-1）in lung cancer A549 cell culture supernatant. After knocking down the MCP-1 expression in lung cancer cells by transfecting shRNA and blocking MCP-1 receptor CCR2 on the surface of HUMSCs by inhibitor RS504393, the migration ability of HUMSCs was determined in vitro and in vivo. Results: HUMSCs were successfully isolated and identified. Subcutaneous lung cancer xenograft model was successfully established in nude BALB/c mice. HUMSCs migrated to lung cancer both in vivo and in vitro（P<0.01）. Lung cancer cells highly expressed MCP-1. Lung cancer A549 cell line with stable low expression of MCP-1 was successfully constructed, compared with control group, number of migrating HUMSCs significantly decreased in shRNA1 and shRNA2 knock down groups （\[80.0±33.0\]，\[94.0±16.0\] vs \[167.0±41.0\]，P<0.05）. Inhibition of CCR2 (receptor of MCP-1) on HUMSCs greatly suppressed the tropism of HUMSCs to lung cancer in vivo and in vitro （P<0.05）. Conclusion: MCP-1/CCR2 axis promoted the migration of HUMSCs to lung cancer.

国家重点基础研究发展计划（973计划）资助项目（No．2012CB9333004）；国家科技支撑计划资助项目（No.2015BAI12B12）；国家自然科学基金资助项目（No. 81401887）；天津市科委应用基础基金资助项目（No. 14JCQNJC11500, No. 11JCYBJC13200）；天津医科大学科学基金资助项目（No. 2012KYM03）