Cancer-associated fibroblast-secreted CXCL16 attracts monocytes to promote stroma activation in triple-negative breast cancers

Roni Allaoui, Caroline Bergenfelz, Sofie Mohlin, Catharina Hagerling, Kiarash Salari, Zena Werb, Robin L. Anderson, Stephen P. Ethier, Karin Jirström, Sven Påhlman, Daniel Bexell, Balázs Tahin, Martin E. Johansson, Christer Larsson and Karin Leandersson ()
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Roni Allaoui: Cancer Immunology, Lund University
Caroline Bergenfelz: Cancer Immunology, Lund University
Sofie Mohlin: Translational Cancer Research, Lund University
Catharina Hagerling: Cancer Immunology, Lund University
Kiarash Salari: University of California
Zena Werb: University of California
Robin L. Anderson: Peter MacCallum Cancer Centre, The University of Melbourne
Stephen P. Ethier: Hollings Cancer Center, Medical University of South Carolina
Karin Jirström: Oncology and Pathology, Lund University
Sven Påhlman: Translational Cancer Research, Lund University
Daniel Bexell: Translational Cancer Research, Lund University
Balázs Tahin: Clinical Pathology, Skånes Universitetssjukhus
Martin E. Johansson: Cancer Immunology, Lund University
Christer Larsson: Translational Cancer Research, Lund University
Karin Leandersson: Cancer Immunology, Lund University

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Triple-negative (TN) breast cancers (ER−PR−HER2−) are highly metastatic and associated with poor prognosis. Within this subtype, invasive, stroma-rich tumours with infiltration of inflammatory cells are even more aggressive. The effect of myeloid cells on reactive stroma formation in TN breast cancer is largely unknown. Here, we show that primary human monocytes have a survival advantage, proliferate in vivo and develop into immunosuppressive myeloid cells expressing the myeloid-derived suppressor cell marker S100A9 only in a TN breast cancer environment. This results in activation of cancer-associated fibroblasts and expression of CXCL16, which we show to be a monocyte chemoattractant. We propose that this migratory feedback loop amplifies the formation of a reactive stroma, contributing to the aggressive phenotype of TN breast tumours. These insights could help select more suitable therapies targeting the stromal component of these tumours, and could aid prediction of drug resistance.

Date: 2016
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DOI: 10.1038/ncomms13050

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