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 Senba, Eiji Kobayashi, Masafumi Takahashi, Takashi Murakami

    研究成果: Article

    42 引用 (Scopus)

    抄録

    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.

    元の言語English
    記事番号e44080
    ジャーナルPLoS One
    7
    発行部数8
    DOI
    出版物ステータスPublished - 2012 8 29

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    Tumors
    Cells
    neoplasms
    Myeloid Cells
    Neoplasms
    cells
    immatures
    chemokines
    angiogenesis
    mice
    neoplasm cells
    CXC Chemokines
    Gastrointestinal Neoplasms
    SCID Mice
    lung neoplasms
    colorectal neoplasms
    Chemokines
    Heterografts
    metastasis
    breast neoplasms

    ASJC Scopus subject areas

    • Agricultural and Biological Sciences(all)
    • Biochemistry, Genetics and Molecular Biology(all)
    • Medicine(all)

    これを引用

    Matsui, A., Yokoo, H., Negishi, Y., Endo-Takahashi, Y., Chun, N. A. L., Kadouchi, I., ... Murakami, T. (2012). CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80- Cells and Promotes Tumor Progression. PLoS One, 7(8), [e44080]. https://doi.org/10.1371/journal.pone.0044080

    CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80- Cells and Promotes Tumor Progression. / Matsui, Aya; Yokoo, Hideaki; Negishi, Yoichi; Endo-Takahashi, Yoko; Chun, Nicole A L; Kadouchi, Ichiro; Suzuki, Ryo; Maruyama, Kazuo; Aramaki, Yukihiko; Senba, Kentaro; Kobayashi, Eiji; Takahashi, Masafumi; Murakami, Takashi.

    :: PLoS One, 巻 7, 番号 8, e44080, 29.08.2012.

    研究成果: Article

    Matsui, A, Yokoo, H, Negishi, Y, Endo-Takahashi, Y, Chun, NAL, Kadouchi, I, Suzuki, R, Maruyama, K, Aramaki, Y, Senba, K, Kobayashi, E, Takahashi, M & Murakami, T 2012, 'CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80- Cells and Promotes Tumor Progression', PLoS One, 巻. 7, 番号 8, e44080. https://doi.org/10.1371/journal.pone.0044080
    Matsui A, Yokoo H, Negishi Y, Endo-Takahashi Y, Chun NAL, Kadouchi I その他. CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80- Cells and Promotes Tumor Progression. PLoS One. 2012 8 29;7(8). e44080. https://doi.org/10.1371/journal.pone.0044080
    Matsui, Aya ; Yokoo, Hideaki ; Negishi, Yoichi ; Endo-Takahashi, Yoko ; Chun, Nicole A L ; Kadouchi, Ichiro ; Suzuki, Ryo ; Maruyama, Kazuo ; Aramaki, Yukihiko ; Senba, Kentaro ; Kobayashi, Eiji ; Takahashi, Masafumi ; Murakami, Takashi. / CXCL17 Expression by Tumor Cells Recruits CD11b+Gr1highF4/80- Cells and Promotes Tumor Progression. :: PLoS One. 2012 ; 巻 7, 番号 8.
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    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+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.",
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    AU - Matsui, Aya

    AU - Yokoo, Hideaki

    AU - Negishi, Yoichi

    AU - Endo-Takahashi, Yoko

    AU - Chun, Nicole A L

    AU - Kadouchi, Ichiro

    AU - Suzuki, Ryo

    AU - Maruyama, Kazuo

    AU - Aramaki, Yukihiko

    AU - Senba, Kentaro

    AU - Kobayashi, Eiji

    AU - Takahashi, Masafumi

    AU - Murakami, Takashi

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