Fig. 3

Cortisol triggers TAMs/CXCL1 signaling in a GR-dependent manner. A The population of CD206⁺-RAW264.7 after gradient cortisol treatment. B The CXCL1 level secreted by M2-polarized RAW264.7 was measured by ELISA assays after cortisol treatment. C The effects of GR antagonist RU486 or GR knockdown on cortisol-induced M2-polarization in RAW264.7 cells. D M2-polarized RAW264.7 cells were treated with GR antagonist RU486 or GR knockdown. The secretion and expression levels of CXCL1 induced by cortisol (200 nM) in M2-type RAW264.7 cells were then detected. E-F 4T1 cells were co-injected with TAMs or GR-knockdown TAMs into the mammary fat pad of mice to investigate the role of GR on cortisol-promoted cancer growth (n = 6), lung colonization (n = 6), and metastatic lesion formation (n = 4). Data are represented as the Mean ± SD. For statistical analysis, unpaired t-tests (C, D, F), one-way ANOVA with Dunnett post hoc test (A, B), and repeated measures analysis of variance (E) were applied. ^*P < 0.05, ^#P < 0.01