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

Author

Listed:
  • 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
    University of California)

  • 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
    Clinical Pathology, Skånes Universitetssjukhus)

  • Christer Larsson

    (Translational Cancer Research, Lund University)

  • Karin Leandersson

    (Cancer Immunology, Lund University)

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.

Suggested Citation

  • 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 Ta, 2016. "Cancer-associated fibroblast-secreted CXCL16 attracts monocytes to promote stroma activation in triple-negative breast cancers," Nature Communications, Nature, vol. 7(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13050
    DOI: 10.1038/ncomms13050
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    Cited by:

    1. Feng Wang & Yunxuan Li & Zhaona Yang & Wenbin Cao & Ying Liu & Luyao Zhao & Tingting Zhang & Chenxi Zhao & Jinmei Yu & Jiaojiao Yu & Jichao Zhou & Xiaowei Zhang & Ping-Ping Li & Mingzhe Han & Sizhou F, 2024. "Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    2. Bhavana Palakurthi & Shaneann R. Fross & Ian H. Guldner & Emilija Aleksandrovic & Xiyu Liu & Anna K. Martino & Qingfei Wang & Ryan A. Neff & Samantha M. Golomb & Cheryl Lewis & Yan Peng & Erin N. Howe, 2023. "Targeting CXCL16 and STAT1 augments immune checkpoint blockade therapy in triple-negative breast cancer," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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