期刊
CANCER CELL
卷 24, 期 5, 页码 631-644出版社
CELL PRESS
DOI: 10.1016/j.ccr.2013.10.009
关键词
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资金
- NIH MERIT [R37 DK47297, RO1 DK 62112]
- NCI [P01 CA77839]
- CPRIT [RP100960]
- National Colorectal Cancer Research Alliance
- Uehara Memorial Foundation Research Fellowship
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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