Melanoma-initiating cells exploit M2 macrophage TGFβ and arginase pathway for survival and proliferation

Abstract : M2 macrophages promote tumor growth and metastasis, but their interactions with specific tumor cell populations are poorly characterized. Using a mouse model of spontaneous melanoma, we showed that CD34 -but not CD34 + tumor-initiating cells (TICs) depend on M2 macrophages for survival and proliferation. Tumor-associated macrophages (TAMs) and macrophage-conditioned media protected CD34 -TICs from chemotherapy in vitro. In vivo, while inhibition of CD115 suppressed the macrophage-dependent CD34 -TIC population, chemotherapy accelerated its development. The ability of TICs to respond to TAMs was acquired during melanoma progression and immediately preceded a surge in metastatic outgrowth. TAM-derived transforming growth factor-β (TGFβ) and polyamines produced via the Arginase pathway were critical for stimulation of TICs and synergized to promote their growth.
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Oncotarget, Impact journals, 2014, pp.25294815
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  • HAL Id : inserm-01078327, version 1
  • PUBMED : 25294815

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Muly Tham, Kar Wai Tan, Jo Keeble, Xiaojie Wang, Sandra Hubert, et al.. Melanoma-initiating cells exploit M2 macrophage TGFβ and arginase pathway for survival and proliferation. Oncotarget, Impact journals, 2014, pp.25294815. 〈inserm-01078327〉

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