CCL18通过促进整合素的聚集增强乳腺癌细胞黏附于细胞外基质  

CCL18 promotes breast cancer cells adherence on extracellular matrix mediated by integrin aggregation

作　　者：陈静琦[1] 朱必胜[1] 侯开连[1] 

机构地区：[1]广州医学院第二附属医院肿瘤科,广东广州510260

出　　处：《中国癌症杂志》2013年第1期26-31,共6页China Oncology

基　　金：国家自然科学基金项目(No:81172537);广州市属高校科技计划项目(No:08A080)

摘　　要：背景与目的:在乳腺癌微环境中,肿瘤相关巨噬细胞(tumor associated macrophages,TAMs)分泌CCL18,CCL18与病人的预后呈负相关。本文旨在探讨来源于TAMs的CCL18是否能促进乳腺癌细胞黏附于细胞外基质(extracellular matrix,ECM),进一步阐明CCL18促进乳腺癌细胞黏附于ECM的分子机制。方法:在无血清培养体系中,用纤粘连蛋白包被培养板,用黏附实验的方法检测CCL18对乳腺癌SK-3rd细胞黏附于ECM的作用;用免疫荧光的方法检测CCL18对SK-3rd细胞表面整合素的影响。结果:CCL18通过引起乳腺癌SK-3rd细胞表面整合素的聚集,导致乳腺癌SK-3rd细胞黏附于ECM的数量明显增多。结论:CCL18通过促进整合素聚集而促进乳腺癌细胞黏附于ECM。Background and purpose： In the microenvironment of breast cancer, tumor associated macrophages （TAMs） secrete CCL18, and CCL 18 has negative correlation with prognosis of patients. The present study investigated whether CCL18 derived from TAMs, promoted breast cancer cells adherence on extracellular matrix （ECM）, and further interpreted the molecular mechanism of CCL18 promoting breast cancer adherence. Methods： In the serum-free culture system of breast cancer cells, in cultivation plate coated with fibronectin, adherence assay was performed to detect CCL 18 function on breast cancer SK-3rd cells to adherence on ECM, and immunofluorescence was carried out to detect CCL 18 influence integrin aggregation on SK-3rd. Results： CCL 18 elevated the number of SK-3^rd breast cancer cells to adherence on ECM, via integrin ct5131 aggregation. Conclusion： CCL18 promotes breast cancer cells adherence on ECM via integrin aggregation.

关 键 词：乳腺癌 CCL18 黏附 细胞外基质 整合素 

分 类 号：R737.9[医药卫生—肿瘤]