Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/79494
Title: Melanoma-initiating cells exploit M2 macrophage TGFβ and arginase pathway for survival and proliferation
Authors: Tan, Kar Wai
Kato, Masashi
Keeble, Jo
Wang, Xiaojie
Hubert, Sandra
Barron, Luke
Tan, Nguan Soon
Angeli, Veronique
Abastado, Jean-Pierre
Tham, Muly
Prevost-Blondel, Armelle
Keywords: DRNTU::Science::Biological sciences
Issue Date: 2014
Source: Tham, M., Tan, K. W., Keeble, Jo., Wang, X., Hubert, S., Barron, L., et al. (2014). Melanoma-initiating cells exploit M2 macrophage TGFβ and arginase pathway for survival and proliferation. Oncotarget, 5(23), 12027-12042.
Series/Report no.: Oncotarget
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.
URI: https://hdl.handle.net/10356/79494
http://hdl.handle.net/10220/24702
ISSN: 1949-2553
Rights: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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