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Fig. 3 | Breast Cancer Research

Fig. 3

From: A positive feedback loop driven by fibronectin and IL-1β sustains the inflammatory microenvironment in breast cancer

Fig. 3

Association of FN-EDA with IL-1β and STAT3 inflammatory pathways. A Correlation of macrophage M2 subtype with FN-EDA expression in breast tumors assessed by using METABRIC data. B Phospho-STAT3 expression was determined in CD68+ macrophages in TNBC tumor specimens. Representative immunofluorescence staining from a patient is shown. C STAT3 phosphorylation (pSTAT3) levels were assessed by Western blot in the monocytes treated with CM from TNBC cell lines. MDA-MB-468 cell line represents the Basal-like A subtype of TNBC. D Correlation analysis of IL-1β and STAT3 gene expression in freshly obtained breast cancer tissues. E IL-1β secretion levels (upper panel) and NF-κB activity (lower panel) in the monocytes incubated with CM from TNBC cell lines in the presence of plasma fibronectin (pFN), recombinant FN lacking EDA domain (rFN-EDA) and recombinant FN with EDA domain (rFN-EDA+) (A.U, arbitrary units). F Inhibition of TNBC CM-induced activation of the STAT3 pathway through stattic treatment was studied by Western blot. The control cells were treated with DMSO, the solvent for stattic. G Decrease in IL-1β secretion (upper panel) and NF-κB activity (lower panel) in the monocytes pre-treated with stattic. The fold change was calculated in comparison to the control monocytes incubated with CM from TNBC cell lines in the presence of the plasma fibronectin (pFN), the recombinant FN lacking the EDA domain (rFN-EDA) and the recombinant FN with the EDA domain (rFN-EDA.+). (A.U, arbitrary units). Each experiment was repeated at least three times with monocytes from different donors. (Mean ± SEM, Student’s t test; *, P < 0.05; **, P < 0.01). (Black bars, monocytes in the control media; blue bars, CM from low-level fibronectin-expressing cell lines; red bars, CM from high-level fibronectin-expressing cell lines)

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