title: CXCL17 expression by tumor cells recruits CD11b+Gr1 high F4/80- cells and promotes tumor progression.
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.
  
  
  RESULTS
  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(+)Gr1(high)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
  These results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis.
authors.affiliation: Laboratory of Tumor Biology, Takasaki University of Health and Welfare, Takasaki, Gunma, Japan.
authors.forename: Aya
authors.initials: A
authors.lastname: Matsui
authors.forename: Hideaki
authors.initials: H
authors.lastname: Yokoo
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Negishi
authors.forename: Yoko
authors.initials: Y
authors.lastname: Endo-Takahashi
authors.forename: Nicole A L
authors.initials: NA
authors.lastname: Chun
authors.forename: Ichiro
authors.initials: I
authors.lastname: Kadouchi
authors.forename: Ryo
authors.initials: R
authors.lastname: Suzuki
authors.forename: Kazuo
authors.initials: K
authors.lastname: Maruyama
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Aramaki
authors.forename: Kentaro
authors.initials: K
authors.lastname: Semba
authors.forename: Eiji
authors.initials: E
authors.lastname: Kobayashi
authors.forename: Masafumi
authors.initials: M
authors.lastname: Takahashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Murakami
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000378:metabolism*; D039481:CD11b Antigen / Q000378:metabolism*; D002454:Cell Differentiation; D045744:Cell Line, Tumor; D002471:Cell Transformation, Neoplastic / Q000378:metabolism / Q000473:pathology*; D019743:Chemokines, CXC / Q000235:genetics / Q000378:metabolism*; D018450:Disease Progression; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D051379:Mice; D022423:Myeloid Cells / Q000473:pathology; D041681:NIH 3T3 Cells; D009369:Neoplasms / Q000098:blood supply / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: D000950:Antigens, Ly; D039481:CD11b Antigen; D019743:Chemokines, CXC; C480309:Ly6G antigen, mouse; D012333:RNA, Messenger