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Snail promotes ovarian cancer progression by recruiting myeloid-derived suppressor cells via CXCR2 ligand upregulation

Author

Listed:
  • Mana Taki

    (Kyoto University Graduate School of Medicine)

  • Kaoru Abiko

    (Kyoto University Graduate School of Medicine)

  • Tsukasa Baba

    (Kyoto University Graduate School of Medicine)

  • Junzo Hamanishi

    (Kyoto University Graduate School of Medicine)

  • Ken Yamaguchi

    (Kyoto University Graduate School of Medicine)

  • Ryusuke Murakami

    (Kyoto University Graduate School of Medicine)

  • Koji Yamanoi

    (Kyoto University Graduate School of Medicine)

  • Naoki Horikawa

    (Kyoto University Graduate School of Medicine)

  • Yuko Hosoe

    (Kyoto University Graduate School of Medicine)

  • Eijiro Nakamura

    (Kyoto University Graduate School of Medicine)

  • Aiko Sugiyama

    (Kyoto University Graduate School of Medicine)

  • Masaki Mandai

    (Kyoto University Graduate School of Medicine)

  • Ikuo Konishi

    (Kyoto University Graduate School of Medicine)

  • Noriomi Matsumura

    (Kyoto University Graduate School of Medicine)

Abstract

Snail is a major transcriptional factor that induces epithelial-mesenchymal transition (EMT). In this study, we explore the effect of Snail on tumor immunity. Snail knockdown in mouse ovarian cancer cells suppresses tumor growth in immunocompetent mice, associated with an increase of CD8+ tumor-infiltrating lymphocytes and a decrease of myeloid-derived suppressor cells (MDSCs). Snail knockdown reduces the expression of CXCR2 ligands (CXCL1 and CXCL2), chemokines that attract MDSCs to the tumor via CXCR2. Snail upregulates CXCR ligands through NF-kB pathway, and most likely, through direct binding to the promoters. A CXCR2 antagonist suppresses MDSC infiltration and delays tumor growth in Snail-expressing mouse tumors. Ovarian cancer patients show elevated serum CXCL1/2, which correlates with Snail expression, MDSC infiltration, and short overall survival. Thus, Snail induces cancer progression via upregulation of CXCR2 ligands and recruitment of MDSCs. Blocking CXCR2 represents an immunological therapeutic approach to inhibit progression of Snail-high tumors undergoing EMT.

Suggested Citation

  • Mana Taki & Kaoru Abiko & Tsukasa Baba & Junzo Hamanishi & Ken Yamaguchi & Ryusuke Murakami & Koji Yamanoi & Naoki Horikawa & Yuko Hosoe & Eijiro Nakamura & Aiko Sugiyama & Masaki Mandai & Ikuo Konish, 2018. "Snail promotes ovarian cancer progression by recruiting myeloid-derived suppressor cells via CXCR2 ligand upregulation," Nature Communications, Nature, vol. 9(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03966-7
    DOI: 10.1038/s41467-018-03966-7
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    Cited by:

    1. Qiming Zhou & Yao Peng & Fenfen Ji & Huarong Chen & Wei Kang & Lam-Shing Chan & Hongyan Gou & Yufeng Lin & Pingmei Huang & Danyu Chen & Qinyao Wei & Hao Su & Cong Liang & Xiang Zhang & Jun Yu & Chi Ch, 2023. "Targeting of SLC25A22 boosts the immunotherapeutic response in KRAS-mutant colorectal cancer," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    2. Peitao Zhang & Haixia Guan & Shukai Yuan & Huili Cheng & Jian Zheng & Zhenlei Zhang & Yifan Liu & Yang Yu & Zhaowei Meng & Xiangqian Zheng & Li Zhao, 2022. "Targeting myeloid derived suppressor cells reverts immune suppression and sensitizes BRAF-mutant papillary thyroid cancer to MAPK inhibitors," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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