Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 210, Issue 9, Pages 1711-1728Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20130440
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Funding
- Association for International Cancer Research (AICR, UK)
- Italian Association for Cancer Research (AIRC)
- Italian Ministry of Health [RF-2009]
- Crohn's & Colitis Foundation of America (CCFA)
- Cancer Research Institute (CRI)
- Howard H. Goodman (MGH)
- Massachusetts Life Science Center (MLSC)
- NIH [DP2 2009A054301]
- Swedish Science Council [522-2008-3745]
- Robert A. Welch Foundation
- Special Program Molecular Clinical Oncology AIRC 5 per mille [9965]
- Worldwide Cancer Research [11-0751] Funding Source: researchfish
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Tumor-infiltrating immune cells can be conditioned by molecules released within the microenvironment to thwart antitumor immune responses, thereby facilitating tumor growth. Among immune cells, neutrophils play an important protumorigenic role by favoring neoangiogenesis and/or by suppressing antitumor immune responses. Tumor-derived oxysterols have recently been shown to favor tumor growth by inhibiting dendritic cell migration toward lymphoid organs. We report that tumor-derived oxysterols recruit protumor neutrophils in a liver X receptor (LXR)-independent, CXCR2-dependent manner, thus favoring tumor growth by promoting neoangiogenesis and immunosuppression. We demonstrate that interfering with the oxysterol-CXCR2 axis delays tumor growth and prolongs the overall survival of tumor-bearing mice. These results identify an unanticipated protumor function of the oxysterol-CXCR2 axis and a possible target for cancer therapy.
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