CXCL1 mediates obesity-associated adipose stromal cell trafficking and function in the tumour microenvironment

Tao Zhang, Chieh Tseng, Yan Zhang, Olga Sirin, Paul G. Corn, Elsa M. Li-Ning-Tapia, Patricia Troncoso, John Davis, Curtis Pettaway, John Ward, Marsha L. Frazier, Christopher Logothetis and Mikhail G. Kolonin ()
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Tao Zhang: The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston
Chieh Tseng: The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston
Yan Zhang: The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston
Olga Sirin: The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston
Paul G. Corn: The University of Texas MD Anderson Cancer Center
Elsa M. Li-Ning-Tapia: The University of Texas MD Anderson Cancer Center
Patricia Troncoso: The University of Texas MD Anderson Cancer Center
John Davis: The University of Texas MD Anderson Cancer Center
Curtis Pettaway: The University of Texas MD Anderson Cancer Center
John Ward: The University of Texas MD Anderson Cancer Center
Marsha L. Frazier: The University of Texas MD Anderson Cancer Center
Christopher Logothetis: The University of Texas MD Anderson Cancer Center
Mikhail G. Kolonin: The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: Abstract White adipose tissue (WAT) overgrowth in obesity is linked with increased aggressiveness of certain cancers. Adipose stromal cells (ASCs) can become mobilized from WAT, recruited by tumours and promote cancer progression. Mechanisms underlying ASC trafficking are unclear. Here we demonstrate that chemokines CXCL1 and CXCL8 chemoattract ASC by signalling through their receptors, CXCR1 and CXCR2, in cell culture models. We further show that obese patients with prostate cancer have increased epithelial CXCL1 expression. Concomitantly, we observe that cells with ASC phenotype are mobilized and infiltrate tumours in obese patients. Using mouse models, we show that the CXCL1 chemokine gradient is required for the obesity-dependent tumour ASC recruitment, vascularization and tumour growth promotion. We demonstrate that αSMA expression in ASCs is induced by chemokine signalling and mediates the stimulatory effects of ASCs on endothelial cells. Our data suggest that ASC recruitment to tumours, driven by CXCL1 and CXCL8, promotes prostate cancer progression.

Date: 2016
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DOI: 10.1038/ncomms11674

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