CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80− Cells and Promotes Tumor Progression
Tumor progression
DOI:
10.1371/journal.pone.0044080
Publication Date:
2012-08-29T21:11:21Z
AUTHORS (13)
ABSTRACT
Background Chemokines are involved in multiple aspects of pathogenesis and cellular trafficking tumorigenesis. In this study, we report that the latest member C-X-C-type chemokines, CXCL17 (DMC/VCC-1), recruits immature myeloid-derived cells enhances early tumor progression. Methodology/Principal Findings was preferentially expressed some aggressive types gastrointestinal, breast, lung cancer cells. expression did not impart NIH3T3 with oncogenic potential vitro, but CXCL17-expressing could form vasculature-rich tumors immunodeficient mice. Our data showed increased CD11b+Gr1+ at sites mice promoted CD31+ angiogenesis. Extensive chemotactic assays proved CXCL17-responding were CD11b+Gr1highF4/80− (∼90%) a neutrophil-like morphology vitro. Although increase number tumor-burdened SCID or promote metastases low metastatic colon cells, existence caused striking enhancement xenograft formation. Conclusions/Significance These results suggest aberrant promotes progression through
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