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Citrullinated fibrinogen-SAAs complex causes vascular metastagenesis

Author

Listed:
  • Yibing Han

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

  • Takeshi Tomita

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

  • Masayoshi Kato

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

  • Norihiro Ashihara

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

  • Yumiko Higuchi

    (Shinshu University
    Shinshu University School of Medicine)

  • Hisanori Matoba

    (Shinshu University School of Medicine)

  • Weiyi Wang

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

  • Hikaru Hayashi

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

  • Yuji Itoh

    (Tohoku University)

  • Satoshi Takahashi

    (Tohoku University)

  • Hiroshi Kurita

    (Shinshu University School of Medicine)

  • Jun Nakayama

    (Shinshu University School of Medicine)

  • Nobuo Okumura

    (Shinshu University
    Shinshu University School of Medicine)

  • Sachie Hiratsuka

    (Shinshu University School of Medicine
    Shinshu University School of Medicine)

Abstract

Primary tumor cells metastasize to a distant preferred organ. However, the most decisive host factors that determine the precise locations of metastases in cancer patients remain unknown. We have demonstrated that post-translational citrullination of fibrinogen creates a metastatic niche in the vulnerable spots. Pulmonary endothelial cells mediate the citrullination of fibrinogen, changing its conformation, surface charge, and binding properties with serum amyloid A proteins (SAAs), to make it a host tissue-derived metastatic pathogen. The human-specific SAAs-citrullinated fibrinogen (CitFbg) complex recruits cancer cells to form a protein-metastatic cell aggregation in humanized SAA cluster mice. Furthermore, a CitFbg peptide works as a competitive inhibitor to block the homing of metastatic cells into the SAAs-CitFbg sites. The potential metastatic sites in the lungs of patients are clearly visualized by our specific antibody for CitFbg. Thus, CitFbg deposition displays metastatic risks for cancer patients, and the citrullinated peptide is a new type of metastasis inhibitor.

Suggested Citation

  • Yibing Han & Takeshi Tomita & Masayoshi Kato & Norihiro Ashihara & Yumiko Higuchi & Hisanori Matoba & Weiyi Wang & Hikaru Hayashi & Yuji Itoh & Satoshi Takahashi & Hiroshi Kurita & Jun Nakayama & Nobu, 2023. "Citrullinated fibrinogen-SAAs complex causes vascular metastagenesis," Nature Communications, Nature, vol. 14(1), pages 1-18, December.
  • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-40371-1
    DOI: 10.1038/s41467-023-40371-1
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    References listed on IDEAS

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    1. Dimitrios Davalos & Jae Kyu Ryu & Mario Merlini & Kim M. Baeten & Natacha Le Moan & Mark A. Petersen & Thomas J. Deerinck & Dimitri S. Smirnoff & Catherine Bedard & Hiroyuki Hakozaki & Sara Gonias Mur, 2012. "Fibrinogen-induced perivascular microglial clustering is required for the development of axonal damage in neuroinflammation," Nature Communications, Nature, vol. 3(1), pages 1-15, January.
    2. Sachie Hiratsuka & Sachie Ishibashi & Takeshi Tomita & Akira Watanabe & Sachiko Akashi-Takamura & Masato Murakami & Hiroshi Kijima & Kensuke Miyake & Hiroyuki Aburatani & Yoshiro Maru, 2013. "Primary tumours modulate innate immune signalling to create pre-metastatic vascular hyperpermeability foci," Nature Communications, Nature, vol. 4(1), pages 1-10, October.
    3. Rosandra N. Kaplan & Rebecca D. Riba & Stergios Zacharoulis & Anna H. Bramley & Loïc Vincent & Carla Costa & Daniel D. MacDonald & David K. Jin & Koji Shido & Scott A. Kerns & Zhenping Zhu & Daniel Hi, 2005. "VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche," Nature, Nature, vol. 438(7069), pages 820-827, December.
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