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Cancer Immunology Research
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Enzalutamide, an Androgen Receptor Antagonist, Enhances Myeloid Cell–Mediated Immune Suppression and Tumor Progression

Camila R. Consiglio, Olga Udartseva, Kimberly D. Ramsey, Chioma Bush and Sandra O. Gollnick
Camila R. Consiglio
1Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
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  • ORCID record for Camila R. Consiglio
Olga Udartseva
2Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
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  • ORCID record for Olga Udartseva
Kimberly D. Ramsey
2Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
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Chioma Bush
2Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
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Sandra O. Gollnick
1Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
2Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
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  • For correspondence: sandra.gollnick@roswellpark.org
DOI: 10.1158/2326-6066.CIR-19-0371 Published September 2020
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Abstract

Androgen receptor (AR) antagonism increases overall survival in prostate cancer; however, treatment failure leads to tumor progression and patient mortality. The effect of AR modulation on AR+ nontumor cells that participate in the resistance to AR antagonism is poorly understood. Tumor-infiltrating myeloid cells, including macrophages and myeloid-derived suppressor cells (MDSC), express AR and promote prostate cancer progression. We investigated how AR antagonism affects myeloid cell function and metabolism in an AR-independent murine colon tumor model. Systemic blockade of AR with enzalutamide resulted in increased MC-38 tumor growth in vivo even when AR was knocked out of MC-38 tumor cells. MC-38 tumor growth was also increased when immunocompetent, but not immunodeficient, mice were coinjected with tumor cells and MDSCs treated with enzalutamide or lacking AR, suggesting that AR regulated the ability of MDSCs to suppress adaptive immunity. Myeloid AR-knockout male mice also displayed increased growth of TRAMP C2 prostate tumors when compared with wild type. Inhibition of AR signaling suppressed mitochondrial respiration in myeloid cells via MPC/AMPK signaling pathways; suppression of mitochondrial respiration increased MDSC tumor–promoting functions. Our work showed that AR regulates a tumor-promoting myeloid cell phenotype and influences myeloid cell metabolism. These findings suggest that tumor resistance to AR antagonism is due, in part, to changes in myeloid cell function and metabolism.

Footnotes

  • Note: Supplementary data for this article are available at Cancer Immunology Research Online (http://cancerimmunolres.aacrjournals.org/).

  • Cancer Immunol Res 2020;8:1215–27

  • Received May 20, 2019.
  • Revision received October 2, 2019.
  • Accepted June 30, 2020.
  • Published first July 13, 2020.
  • ©2020 American Association for Cancer Research.
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Cancer Immunology Research: 8 (9)
September 2020
Volume 8, Issue 9
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Enzalutamide, an Androgen Receptor Antagonist, Enhances Myeloid Cell–Mediated Immune Suppression and Tumor Progression
Camila R. Consiglio, Olga Udartseva, Kimberly D. Ramsey, Chioma Bush and Sandra O. Gollnick
Cancer Immunol Res September 1 2020 (8) (9) 1215-1227; DOI: 10.1158/2326-6066.CIR-19-0371

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Enzalutamide, an Androgen Receptor Antagonist, Enhances Myeloid Cell–Mediated Immune Suppression and Tumor Progression
Camila R. Consiglio, Olga Udartseva, Kimberly D. Ramsey, Chioma Bush and Sandra O. Gollnick
Cancer Immunol Res September 1 2020 (8) (9) 1215-1227; DOI: 10.1158/2326-6066.CIR-19-0371
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