Fig. 4: CXCL12–CXCR4 axis induces AKT-mediated β-catenin activation in CXCR4⁺ mammary gland macrophages.

a Pathway enrichment analysis from differentially expressed genes in CXCL12-treated versus non-treated control Mϕ. b, c Flow cytometry histogram presentation of the expression and mean fluorescent intensity (MFI) of phosphorylated-AKT (b) and phosphorylated-β-catenin (Ser⁵⁵²) (c) in CXCR4⁺ and CXCR4⁻ mammary gland macrophages (n = 4, 3, biologically independent samples). d, f Flow cytometry histogram presentation of the expression of phosphorylated-AKT (d) and phosphorylated-β-catenin (Ser⁵⁵²) (f) in mammary gland macrophages cultured in vitro with 200 ng/ml recombinant CXCL12 (rCXCL12), 10 μM AKT inhibitor, GSK690693 (GSK) and 10 μM CXCR4 inhibitor AMD3100 (AMD). e, g MFI of phosphorylated-AKT (e) and phosphorylated-β-catenin (Ser⁵⁵²) (g) in macrophages with different treatment conditions measured by flow cytometry analysis (n = 3, biologically independent samples). h IF co-staining of F4/80 with phosphorylated-β-catenin (Ser⁵⁵²) in littermate control, CXCL12^K8-cKO and CXCR4^Mϕ-cKO mammary glands. The enlargement of areas marked by dashed line boxes is shown on the right panels. White arrows indicated double-positive cells. Scale bar, 50 μm in (h). Flow cytometry analysis of Mϕ gate (Supplementary Fig. 16b) for MFI quantification in (b–g). Data are presented as mean values  ±  s.d. Statistical significance was calculated by two-tailed unpaired Student’s t-test or one-way ANOVA with Turkey’s multiple comparisons test. Source data are provided as a Source Data file.