Macrophages are exploited from an innate wound healing response to facilitate cancer metastasis

Tamara Muliaditan, Jonathan Caron, Mary Okesola, James W. Opzoomer, Paris Kosti, Mirella Georgouli, Peter Gordon, Sharanpreet Lall, Desislava M. Kuzeva, Luisa Pedro, Jacqueline D. Shields, Cheryl E. Gillett, Sandra S. Diebold, Victoria Sanz-Moreno, Tony Ng, Esther Hoste and James N. Arnold ()
Additional contact information
Tamara Muliaditan: Guy’s Campus
Jonathan Caron: Guy’s Campus
Mary Okesola: Guy’s Campus
James W. Opzoomer: Guy’s Campus
Paris Kosti: Guy’s Campus
Mirella Georgouli: Guy′s Campus
Peter Gordon: Guy’s Campus
Sharanpreet Lall: Guy’s Campus
Desislava M. Kuzeva: Guy’s Campus
Luisa Pedro: Hutchison/Medical Research Council Research Centre
Jacqueline D. Shields: Hutchison/Medical Research Council Research Centre
Cheryl E. Gillett: Guy’s Campus
Sandra S. Diebold: National Institute for Biological Standards and Control
Victoria Sanz-Moreno: Guy′s Campus
Tony Ng: Guy’s Campus
Esther Hoste: VIB Center for Inflammation Research
James N. Arnold: Guy’s Campus

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract Tumour-associated macrophages (TAMs) play an important role in tumour progression, which is facilitated by their ability to respond to environmental cues. Here we report, using murine models of breast cancer, that TAMs expressing fibroblast activation protein alpha (FAP) and haem oxygenase-1 (HO-1), which are also found in human breast cancer, represent a macrophage phenotype similar to that observed during the wound healing response. Importantly, the expression of a wound-like cytokine response within the tumour is clinically associated with poor prognosis in a variety of cancers. We show that co-expression of FAP and HO-1 in macrophages results from an innate early regenerative response driven by IL-6, which both directly regulates HO-1 expression and licenses FAP expression in a skin-like collagen-rich environment. We show that tumours can exploit this response to facilitate transendothelial migration and metastatic spread of the disease, which can be pharmacologically targeted using a clinically relevant HO-1 inhibitor.

Date: 2018
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DOI: 10.1038/s41467-018-05346-7

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