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Platelets Promote Metastasis via Binding Tumor CD97 Leading to Bidirectional Signaling that Coordinates Transendothelial Migration

  1. Author:
    Ward, Yvona
    Lake, Ross
    Faraji, Farhoud
    Sperger, Jamie
    Martin, Philip
    Gilliard, Cameron
    Ku, Kimberly P
    Rodems, Tamara
    Niles, David
    Tillman, Heather
    Yin, JuanJuan
    Hunter, Kent
    Sowalsky, Adam G
    Lang, Joshua
    Kelly, Kathleen

  2. Author Address

    Laboratory of Genitourinary Cancer Pathogenesis, NCI, Bethesda, MD 20892, USA., Laboratory of Cancer Biology and Genetics, NCI, Bethesda, MD 20892, USA., Carbone Cancer Center, University of Wisconsin-Madison, Madison, WI 53705, USA., Center for Advanced Preclinical Research, NCI, Frederick, MD 21702, USA., Molecular Biology and Genetics Section, NIDDK, Bethesda, MD 20892, USA., Depatment of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI 53705, USA., Laboratory of Genitourinary Cancer Pathogenesis, NCI, Bethesda, MD 20892, USA. Electronic address: kellyka@mail.nih.gov.,
    1. Year: 2018
    2. Date: Apr 17
  2. Journal: Cell Reports
    1. 23
    2. 3
    3. Pages: 808-822
  4. Type of Article: Article
  5. ISSN: 2211-1247
  1. Abstract:

    Tumor cells initiate platelet activation leading to the secretion of bioactive molecules, which promote metastasis. Platelet receptors on tumors have not been well-characterized, resulting in a critical gap in knowledge concerning platelet-promoted metastasis. We identify a direct interaction between platelets and tumor CD97 that stimulates rapid bidirectional signaling. CD97, an adhesion G protein-coupled receptor (GPCR), is an overexpressed tumor antigen in several cancer types. Purified CD97 extracellular domain or tumor cell-associated CD97 stimulated platelet activation. CD97-initiated platelet activation led to granule secretion, including the release of ATP, a mediator of endothelial junction disruption. Lysophosphatidic acid (LPA) derived from platelets induced tumor invasiveness via proximal CD97-LPAR heterodimer signaling, coupling coincident tumor cell migration and vascular permeability to promote transendothelial migration. Consistent with this, CD97 was necessary for tumor cell-induced vascular permeability in vivo and metastasis formation in preclinical models. These findings support targeted blockade of tumor CD97 as an approach to ameliorate metastatic spread. Published by Elsevier Inc.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.celrep.2018.03.092
  3. PMID: 29669286
  4. View record in Web of Science®
  5. WOS: 000430384900015
  6. PII : S2211-1247(18)30453-4

Library Notes

  1. Fiscal Year: FY2017-2018
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