女性乳腺癌是一种常见的恶性肿瘤，其5年生存率仍然较低。介质亚基1（MED1）基因与巨噬细胞表型转化之间的相关性可能是影响癌症治疗效果的关键因素。本研究拟探讨MED1在巨噬细胞极化中的作用及其对乳腺癌恶性行为的进一步影响。进行生物信息学分析以预测MED1在乳腺癌中的表达模式。流式细胞术用于检测MED1过表达或沉默对巨噬细胞极化的影响。酶联免疫吸附实验用于分析异常MED1表达对巨噬细胞细胞因子分泌的影响。CCK-8、集落形成、Transwell和划痕愈合实验用于研究巨噬细胞条件培养基对乳腺癌细胞恶性行为的影响。MED1表达在M2巨噬细胞中显著增加，MED1过表达显著增加了肿瘤相关巨噬细胞（TAMs）的M2极化和IL-10细胞因子水平。与此同时，MED1过表达的M2巨噬细胞可以显著促进乳腺癌细胞的恶性行为。Dasatinib救助实验证实，MED1诱导的M2巨噬细胞极化可以促进乳腺癌细胞的恶性进展。总之，MED1可以诱导M2巨噬细胞极化，从而调节乳腺癌细胞的恶性行为。 © 2023. 作者授予遗传学出版社独家许可。

Breast cancer is a common malignant tumor in female, and its 5-year survival rate remains low. The correlation between mediator subunit 1 (MED1) gene and macrophage phenotypic transformation may be a key factor affecting the therapeutic effect on cancer.The present study intended to explore the role of MED1 in macrophage polarization and its further influence on the malignant behaviors of breast cancer.Bioinformatics analysis was carried out to predict the expression pattern of MED1 in breast cancer. Flow cytometry was conducted to detect the effect of MED1 overexpression or silencing on macrophage polarization. ELISA was applied to analyze the effect of abnormal MED1 expression on cytokine secretion of macrophages. CCK-8, colony formation, Transwell and scratch healing assays were applied to investigate the effects of macrophage conditioned medium on the malignant behaviors of breast cancer cells.MED1 expression was prominently increased in M2 macrophages, and overexpression of MED1 significantly increased M2 polarization of tumor-associated macrophages (TAMs) and IL-10 cytokine level. Meanwhile, M2 macrophages with MED1 overexpression could significantly promote the malignant behaviors of breast cancer cells. Dasatinib rescue experiment further confirmed that MED1-induced M2 macrophage polarization could facilitate the malignant progression of breast cancer cells.In summary, MED1 could induce M2 macrophage polarization and thus regulate the malignant behaviors of breast cancer cells.© 2023. The Author(s) under exclusive licence to The Genetics Society of Korea.