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机构地区:[1]广州医科大学附属第二医院肿瘤科,广东广州510260
出 处:《重庆医学》2014年第12期1419-1421,共3页Chongqing medicine
基 金:国家自然科学基金资助项目(81272900);广州市属高校科技计划资助项目(08A080)
摘 要:目的探讨整合素在CCL18促进乳腺癌SK-3rd细胞浸润和迁移过程中的作用,以阐明CCL18促进乳腺癌细胞浸润和迁移的分子机制。方法用流式细胞检测技术检测CCL18作用下乳腺癌SK-3rd细胞表面整合素的聚集;采用Western blot检测黏着斑激酶(FAK)的激活;用浸润迁移实验检测乳腺癌SK-3rd细胞的浸润迁移。用siRNA转染检测沉默SK-3rd细胞整合素β1的表达。结果 CCL18促进乳腺癌SK-3rd细胞表面整合素的聚集;从而促进整合素介导的FAK磷酸化激活。在CCL18作用下,乳腺癌SK-3rd细胞浸润和迁移的细胞数增多10倍(P<0.01);用siRNA转染检测沉默SK-3rd细胞整合素β1的表达,可以使CCL18作用下的SK-3rd细胞浸润和迁移数量明显减少。结论 CCL18通过整合素聚集可促进乳腺癌细胞浸润和迁移。Objective To explore the role of integrin in CCL18 for promoting breast cancer SK-3 rd cells invasion and migration process to illuminate the molecular mechanism of CCL 18 for promoting breast cancer SK-3 rd cells invasion and migration process . Methods The flow cytometry was adopted to detect CCL18-induced integrin aggregation ;Western blot was used to detect the focal adhesion kinase(FAK ) activation ,the infiltrating migrationin experiment was adopted to determine the invasion and migration of SK-3rd cells and the siRNAs transfection was used to detect the expression of silence integrin β1 .Results CCL18 promoted the in-tegrinβ1 aggregation in breast cancer SK-3rd cell surface and further promoted the integrin-mediated phosphorylated activation of FAK .Under the reaction of CCL18 ,the cells number of SK-3rd cellular invasion and migration was increased by ten times (P&lt;0 .01) ,which was obviously decreased by siRNA silenced integrin β1 .Conclusion CCL18 promotes breast cancer invasion and mi-gration via integrin aggregation .
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