Abstract: 【Abstract】 Objective To investigate the expression and roles of miR?223 in regulating M2 polarization of macrophage. Methods The expression of miR?223 was detected by using qPCR. The phenotype of miR?223 adjusted macrophage was assayed by flow cytometry and Elisa. The ability of MDA?MB?231 cell migration was evaluated by transwell and wound?healing assay. Results MiR?223 was highly expressed in monocytes than in breast cancer cells. The expression of miR?223 was downregulated during monocytes differentiation stimulated by Lipopolysaccharides （LPS），IL?4 or cocultured with MDA?MB?231 cells. And the extent of miR?223 decrease in IL?4 and coculture group was greater than that in LPS treated group. Knockdown of miR?223 level increasesd the expression of M2 type macrophage markers CCL18，IL?10 and CD206，as well as the motility of cocultured MDA?MB?231 cells. Conclusion MiR?223 could serve as a potential target to improve tumor microenvironment and prevent breast tumor metastasis.

Key words: macrophage, microrna?223, breast cancer

摘要： 【摘要】目的 观察microRNA?223（miR?223）在巨噬细胞M2型激活中的表达及作用。方法 运用慢病毒载体感染的方式在巨噬细胞中过表达或敲低miR?223的表达；应用qPCR检测不同激活状态及转染状态巨噬细胞中miR?223的表达；应用Elisa及流式细胞术检测M2型巨噬细胞的激活状态；应用Transwell迁移实验和划痕实验检测乳腺肿瘤细胞的迁移情况。结果 miR?223在单核/巨噬细胞中的表达明显高于肿瘤细胞，在单核细胞向巨噬细胞分化过程中miR?223表达下调，且IL?4或与肿瘤细胞共培养激活的巨噬细胞下调显著。敲低miR?223的表达而不是增加其表达能够促进M2型巨噬细胞标记物CCL18、IL?10和CD206的表达，并促进共培养肿瘤细胞的迁移。结论 miR?223可作为靶向肿瘤微环境调控肿瘤转移的靶点。

关键词: 乳腺肿瘤 , microRNA?223, 巨噬细胞