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Mass consists of tumor-associated macrophages (TAMs) and poor prognosis is associated with elevated levels of TAMs [44]. Stimuli in the tumor environment polarize TAMs towards a protumor M2 rather than an anti-tumor M1 phenotype [45]. TGF- promotes tumor progression by recruiting TAMs to compete with dendritic cells by suppressing their antigen-presentation [34]. Zhang et al. provide evidence that
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Cer [8]. The observation that miR-634 is able to regulate multiple Ras-MAPK pathway genes instead of one key mediator is thought-provoking. Interestingly, many miRNAs appear to synergistically regulate a set of genes that participate in similar processes, such as the miR-17-cluster (regulates genes involved in growth control) [23], let-7 (represses Ras and its downstream target HMGA2) [24, 25] and
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Cer [8]. The observation that miR-634 is able to regulate multiple Ras-MAPK pathway genes instead of one key mediator is thought-provoking. Interestingly, many miRNAs appear to synergistically regulate a set of genes that participate in similar processes, such as the miR-17-cluster (regulates genes involved in growth control) [23], let-7 (represses Ras and its downstream target HMGA2) [24, 25] and
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Line resulted in decreased EGR2 expression (26). Chandra et al. demonstrate that the MAPK/ERK pathway is a major downstream signaling pathway mediating the stimulatory effects of EGF on EGR2 expression and osteoprogenitor survival [28]. Finally, To et al. report that the same MEK inhibitor utilized in our experiments, U0126, was the elicited the most potent inhibition of EGR2 transcription in brea
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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
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