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000127975 037__ $$aDKFZ-2017-03997
000127975 041__ $$aeng
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000127975 1001_ $$aLu, Haihui$$b0
000127975 245__ $$aA breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages.
000127975 260__ $$aNew York, NY$$bNature America$$c2014
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000127975 520__ $$aThe cell-biological program termed the epithelial-mesenchymal transition (EMT) confers on cancer cells mesenchymal traits and an ability to enter the cancer stem cell (CSC) state. However, the interactions between CSCs and their surrounding microenvironment are poorly understood. Here we show that tumour-associated monocytes and macrophages (TAMs) create a CSC niche through juxtacrine signalling with CSCs. We performed quantitative proteomic profiling and found that the EMT program upregulates the expression of CD90, also known as Thy1, and EphA4, which mediate the physical interactions of CSCs with TAMs by directly binding with their respective counter-receptors on these cells. In response, the EphA4 receptor on the carcinoma cells activates Src and NF-κB. In turn, NF-κB in the CSCs induces the secretion of a variety of cytokines that serve to sustain the stem cell state. Indeed, admixed macrophages enhance the CSC activities of carcinoma cells. These findings underscore the significance of TAMs as important components of the CSC niche.
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000127975 7001_ $$aClauser, Karl R$$b1
000127975 7001_ $$aTam, Wai Leong$$b2
000127975 7001_ $$0P:(DE-HGF)0$$aFröse, Julia$$b3
000127975 7001_ $$aYe, Xin$$b4
000127975 7001_ $$aEaton, Elinor Ng$$b5
000127975 7001_ $$aReinhardt, Ferenc$$b6
000127975 7001_ $$aDonnenberg, Vera S$$b7
000127975 7001_ $$aBhargava, Rohit$$b8
000127975 7001_ $$aCarr, Steven A$$b9
000127975 7001_ $$aWeinberg, Robert A$$b10
000127975 773__ $$0PERI:(DE-600)1494945-3$$a10.1038/ncb3041$$gVol. 16, no. 11, p. 1105 - 1117$$n11$$p1105 - 1117$$tNature cell biology$$v16$$x1476-4679$$y2014
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000127975 9141_ $$y2014
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