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Stimulated M2 polarization. Moreover, human explant mammary gland cultures treated with rSFRP1 show a marked reduction in the human M2 marker, CD163. CD163 is a monocyte/macrophage-restricted scavenge receptor [47] and the mechanism by which rSFRP1 reduces CD163 expression may be due in part to repression of Wnt signaling because Bergenfelz et al. show that breast cancer CD163+ TAMs correlate with
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Stimulated M2 polarization. Moreover, human explant mammary gland cultures treated with rSFRP1 show a marked reduction in the human M2 marker, CD163. CD163 is a monocyte/macrophage-restricted scavenge receptor [47] and the mechanism by which rSFRP1 reduces CD163 expression may be due in part to repression of Wnt signaling because Bergenfelz et al. show that breast cancer CD163+ TAMs correlate with
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Imulates and TGFBR inhibition represses EGR2 mRNA expression in both HMECs as well as MMECs (Additional file 2: Figure S2, Fig. 2). We have also observed that tumors derived from Sfrp1-/- mice express significantly higher levels of both Tgfb1 and Egr2 mRNA (data not shown). Dillon et al. revealed that Egr2 expression is upregulated in Erbb2 driven mammary tumors [25]. However, these researchers di
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MRNA expression of CD163 (left panal) and M1 polarization was evaluated by HLA-DRA mRNA expression (right panal). b Explant mammary gland sections were subjected to immunohistochemical analysis, stained for CD163 (left panel) or HLA-DRA (right panel) and images were captured at 100X. Representative pictures are displayed for tissues from each treatment group which was performed in triplicate sampl
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MRNA expression of CD163 (left panal) and M1 polarization was evaluated by HLA-DRA mRNA expression (right panal). b Explant mammary gland sections were subjected to immunohistochemical analysis, stained for CD163 (left panel) or HLA-DRA (right panel) and images were captured at 100X. Representative pictures are displayed for tissues from each treatment group which was performed in triplicate sampl
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Ated with cancer growth and proliferation. Our data reveal that mouse macrophages polarized to M1 macrophages in response to LPS exhibit a significant increase in M1 marker expression when treated with recombinant SFRP1. The fact that we did not observe similar findings when human mammary gland explants were treated with SFRP1 could be due to the fact that our murine macrophages were isolated from
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Tion, and additional tumor initiating pathways promote mammary carcinogenesis. We have previously shown that activated ERK1/2 levels and the migratory action of TERT-siSFRP1 cells are drastically reduced in response to TGF-R inhibition which is consistent with work described by Imamichi et al. showing that TGF- signaling mediates the cellular migration of breast cancer cells by ERK1/2 activation [
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Tion, and additional tumor initiating pathways promote mammary carcinogenesis. We have previously shown that activated ERK1/2 levels and the migratory action of TERT-siSFRP1 cells are drastically reduced in response to TGF-R inhibition which is consistent with work described by Imamichi et al. showing that TGF- signaling mediates the cellular migration of breast cancer cells by ERK1/2 activation [
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Ated with cancer growth and proliferation. Our data reveal that mouse macrophages polarized to M1 macrophages in response to LPS exhibit a significant increase in M1 marker expression when treated with recombinant SFRP1. The fact that we did not observe similar findings when human mammary gland explants were treated with SFRP1 could be due to the fact that our murine macrophages were isolated from
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Noted in atypical breast lesions [49, 50]. Our studies suggest that loss of SFRP1 in epithelial cells can enhance TGF- mediated EGR2 expression and affect TGF- induced M2 polarization of macrophages. As M2 macrophages secrete growth factors, such as Wnt ligands and EGF, this could contribute to tumor progression through a feed forward cross talk between the epithelium and the immune system. Additi