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

Hiroshi Katoh, Dingzhi Wang, Takiko Daikoku, Haiyan Sun, Sudhansu K. Dey, Raymond N. DuBois

    Research output: Contribution to journalArticle

    209 Scopus citations

    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+ Tcell cytotoxic activity.

    Original languageEnglish (US)
    Pages (from-to)631-644
    Number of pages14
    JournalCancer cell
    Volume24
    Issue number5
    DOIs
    StatePublished - Nov 11 2013

    ASJC Scopus subject areas

    • Oncology
    • Cell Biology
    • Cancer Research

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