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

Muly Tham*, Kar Wai Tan, Jo Keeble, Xiaojie Wang, Sandra Hubert, Luke Barron, Nguan Soon Tan, Masashi Kato, Armelle Prevost-Blondel, Veronique Angeli, Jean Pierre Abastado

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

42 Citations (Scopus)

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 macrophagedependent 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.

Original languageEnglish
Pages (from-to)12027-12042
Number of pages16
JournalOncotarget
Volume5
Issue number23
DOIs
Publication statusPublished - 2014
Externally publishedYes

ASJC Scopus Subject Areas

  • Oncology

Keywords

  • Arginase
  • Macrophages
  • TGFβ
  • Tumor-initiating cell

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