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- Title
CXCL17 Expression by Tumor Cells Recruits CD11b<sup>+</sup>Gr1<sup>high</sup>F4/80<sup>-</sup> Cells and Promotes Tumor Progression.
- Authors
Matsui, Aya; Yokoo, Hideaki; Negishi, Yoichi; Endo.-Takahashi, Yoko; Chun, Nicole A. L.; Kadouchi, Ichiro; Suzuki, Ryo; Maruyama, Kazuo; Aramaki, Yukihiko; Semba, Kentaro; Kobayashi, Eiji; Takahashi, Masafumi; Murakami, Takashi; Pal, Soumitro
- Abstract
Background: Chemokines are involved in multiple aspects of pathogenesis and cellular trafficking in tumorigenesis. In this study, we report that the latest member of the C-X-C-type chemokines, CXCL17 (DMC/VCC-1), recruits immature myeloid-derived cells and enhances early tumor progression. Methodology/Principal Findings: CXCL17 was preferentially expressed in some aggressive types of gastrointestinal, breast, and lung cancer cells. CXCL17 expression did not impart NIH3T3 cells with oncogenic potential in vitro, but CXCL17- expressing NIH3T3 cells could form vasculature-rich tumors in immunodeficient mice. Our data showed that CXCL17-expressing tumor cells increased immature CD11b+ Gr1+ myeloid-derived cells at tumor sites in mice and promoted CD31+ tumor angiogenesis. Extensive chemotactic assays proved that CXCL17-responding cells were CD11b+ Gr1high F4/80- cells (~90%) with a neutrophil-like morphology in vitro. Although CXCL17 expression could not increase the number of CD11b+ Gr1+ cells in tumor-burdened SCID mice or promote metastases of low metastatic colon cancer cells, the existence of CXCL17- responding myeloid-derived cells caused a striking enhancement of xenograft tumor formation. Conclusions/Significance: These results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis.
- Subjects
CHEMOKINES; CARCINOGENESIS; CANCER invasiveness; CANCER cells; TUMORS; METASTASIS
- Publication
PLoS ONE, 2012, Vol 7, Issue 8, p1
- ISSN
1932-6203
- Publication type
Article
- DOI
10.1371/journal.pone.0044080