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CXCR2-Expressing Myeloid-Derived Suppressor Cells Are Essential to Promote Colitis-Associated Tumorigenesis

descriptionPublicationkeyboard_double_arrow_right Article 01 Nov 2013 English Publisher:Elsevier BVJournal:Cancer Cell, volume 24, pages 631-644 (issn: 1535-6108,

Copyright policy )Funded by:NIH | Nuclear Hormone Receptors..., NIH | Eicosanoids and Intestina..., NIH | COX-1 as a Target for Ova...

Authors: Haiyan Sun; Hiroshi Katoh; Dingzhi Wang; Takiko Daikoku; Raymond N. DuBois; Raymond N. DuBois; Sudhansu K. Dey;

doi: 10.1016/j.ccr.2013.10.009

pmid: 24229710

pmc: PMC3928012

CXCR2-Expressing Myeloid-Derived Suppressor Cells Are Essential to Promote Colitis-Associated Tumorigenesis

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Abstract

A large body of evidence indicates that chronic inflammation is one of several key risk factors for cancer initiation, progression, and metastasis. However, the underlying mechanisms responsible for the contribution of inflammation and inflammatory mediators to cancer remain elusive. Here, we present genetic evidence that loss of CXCR2 dramatically suppresses chronic colonic inflammation and colitis-associated tumorigenesis through inhibiting infiltration of myeloid-derived suppressor cells (MDSCs) into colonic mucosa and tumors in a mouse model of colitis-associated cancer. CXCR2 ligands were elevated in inflamed colonic mucosa and tumors and induced MDSC chemotaxis. Adoptive transfer of wild-type MDSCs into Cxcr2(-/-) mice restored AOM/DSS-induced tumor progression. MDSCs accelerated tumor growth by inhibiting CD8(+) T cell cytotoxic activity.

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Keywords

Cytotoxicity, Immunologic, Cancer Research, Carcinogenesis, Chemokine CXCL1, Azoxymethane, CD8-Positive T-Lymphocytes, Dinoprostone, Mice, Animals, Humans, Myeloid Cells, Intestinal Mucosa, Cells, Cultured, Mice, Knockout, Mice, Inbred BALB C, Chemotaxis, Dextran Sulfate, Cell Biology, Colitis, Adoptive Transfer, Oncology, Inflammation Mediators, Colorectal Neoplasms

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