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.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Katoh H,Wang D,Daikoku T,Sun H,Dey SK,Dubois RNdoi
10.1016/j.ccr.2013.10.009subject
Has Abstractpub_date
2013-11-11 00:00:00pages
631-44issue
5eissn
1535-6108issn
1878-3686pii
S1535-6108(13)00457-1journal_volume
24pub_type
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