IRF7
基因敲除
细胞生长
癌症研究
肿瘤进展
巨噬细胞
乳腺癌
癌变
癌症
生物
医学
免疫学
细胞凋亡
内科学
免疫系统
体外
生物化学
遗传学
先天免疫系统
作者
Daoyuan Tu,Jin Dou,Mingkao Wang,Haiwen Zhuang,Xiaoyu Zhang
摘要
Abstract Breast cancer is a kind of malignant tumor that severely threatens women's lives and health worldwide. Tumor‐associated macrophages (TAMs) have been reported to mediate tumor progression, while the mechanism still needs further identification. In this study, we found that M2 macrophages promoted increased cell proliferation and migration as well as reduced expression of interferon regulatory factor 7 (IRF7) and increased the expression of miR‐1587 in breast cancer cells. Overexpression of IRF7 or miR‐1587 knockdown reversed M2 macrophage‐induced cell proliferation and migration as well as tumor growth in vivo. Mechanistically, miR‐1587 targeted the 3ʹ‐untranslated region (3ʹ‐UTR) of IRF7 mRNA to regulate its protein expression leading to tumor progression. Collectively, this study revealed that the miR‐1587/IRF7 axis mediates M2 macrophage‐induced breast cancer progression, and this sheds light on further clinical therapy for breast cancer by targeting TAMs as well as the miR‐1587/IRF7 axis.
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