CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80- Cells and Promotes Tumor Progression

Aya Matsui, Hideaki Yokoo, Yoichi Negishi, Yoko Endo-Takahashi, Nicole A.L. Chun, Ichiro Kadouchi, Ryo Suzuki, Kazuo Maruyama, Yukihiko Aramaki, Kentaro Semba, Eiji Kobayashi, Masafumi Takahashi, Takashi Murakami*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

59 Citations (Scopus)


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+Gr1highF4/80- 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.

Original languageEnglish
Article numbere44080
JournalPloS one
Issue number8
Publication statusPublished - 2012 Aug 29

ASJC Scopus subject areas

  • General


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