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.

Graphical abstractThis figure shows the histological section of the perforated ileal segment. H & E, x100, which indicates the chronic inflammation of the mucosa with erosion, bleeding and infiltration of lymphocytes and neutrophils,this together with the patient history of suffering just a minimal injury to the hernia makes us speculate, that the pathological changes of the intestine in the hernia sac tending to be broken may be one of the crucial factors causing this rare,acute and serious situation. This further highlights the necessity of repairing the inguinal hernia as early as possible.

Background: Breast cancer is a kind of malignant tumor that severely threatens women’s health and life worldwide. Macrophages have been reported to mediate tumor progression, while the potential mechanism still needs further identification.Methods: Human monocytic cell line THP-1 was used to induce M2-macrophage. Real-time PCR and western blot were performed to determine gene expression in mRNA and protein level, respectively. Cell proliferation was determined using MTT assays, while cell migration was detected based on the scratch wound healing assays.Results: The supernatant medium of M2-macrophages incubated breast cancer cells showed increased cell proliferation and reduced expression of IRF-7. Overexpression of IRF-7 reversed the increased level of M2-macrophage induced cell proliferation and migration. The supernatant medium of M2-macrophages incubation promoted miR-1587 expression in breast cancer cells. miR-1587 overexpression promoted cell proliferation and migration of breast cancer. In addition, miR-1587 knockdown suppressed cell proliferation and migration that induced by M2-macrophages. miR-1587 targets IRF-7 to regulate its expression. Knockdown of IRF-7 reversed the effects of miR-1587 knockdown on cell proliferation and migration.Conclusion: Collectively, this study revealed that miR-1587/IRF-7 mediated the mechanism of M2-macrophages-induced breast cancer progression, and this would shed light on the further clinical therapy of breast cancer.