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The CXCL5/CXCR2 axis is sufficient to promote breast cancer colonization during bone metastasis

Author

Listed:
  • Ricardo Romero-Moreno

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Kimberly J. Curtis

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Thomas R. Coughlin

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Maria Cristina Miranda-Vergara

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Shourik Dutta

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Aishwarya Natarajan

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Beth A. Facchine

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Kristen M. Jackson

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Lukas Nystrom

    (Loyola University Medical Center, Stritch School of Medicine
    Cleveland Clinic)

  • Jun Li

    (Harper Cancer Research Institute
    University of Notre Dame)

  • William Kaliney

    (Harper Cancer Research Institute)

  • Glen L. Niebur

    (Harper Cancer Research Institute
    University of Notre Dame)

  • Laurie E. Littlepage

    (Harper Cancer Research Institute
    University of Notre Dame)

Abstract

Bone is one of the most common sites for metastasis across cancers. Cancer cells that travel through the vasculature and invade new tissues can remain in a non-proliferative dormant state for years before colonizing the metastatic site. Switching from dormancy to colonization is the rate-limiting step of bone metastasis. Here we develop an ex vivo co-culture method to grow cancer cells in mouse bones to assess cancer cell proliferation using healthy or cancer-primed bones. Profiling soluble factors from conditioned media identifies the chemokine CXCL5 as a candidate to induce metastatic colonization. Additional studies using CXCL5 recombinant protein suggest that CXCL5 is sufficient to promote breast cancer cell proliferation and colonization in bone, while inhibition of its receptor CXCR2 with an antagonist blocks proliferation of metastatic cancer cells. This study suggests that CXCL5 and CXCR2 inhibitors may have efficacy in treating metastatic bone tumors dependent on the CXCL5/CXCR2 axis.

Suggested Citation

  • Ricardo Romero-Moreno & Kimberly J. Curtis & Thomas R. Coughlin & Maria Cristina Miranda-Vergara & Shourik Dutta & Aishwarya Natarajan & Beth A. Facchine & Kristen M. Jackson & Lukas Nystrom & Jun Li , 2019. "The CXCL5/CXCR2 axis is sufficient to promote breast cancer colonization during bone metastasis," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-12108-6
    DOI: 10.1038/s41467-019-12108-6
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    Cited by:

    1. Jeppe Sejerø Holm & Samuel A. Funt & Annie Borch & Kamilla Kjærgaard Munk & Anne-Mette Bjerregaard & James L. Reading & Colleen Maher & Ashley Regazzi & Phillip Wong & Hikmat Al-Ahmadie & Gopa Iyer & , 2022. "Neoantigen-specific CD8 T cell responses in the peripheral blood following PD-L1 blockade might predict therapy outcome in metastatic urothelial carcinoma," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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