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Seneca Valley Virus Exploits TEM8, a Collagen Receptor Implicated in Tumor Growth

  1. Author:
    Evans, David J.
    Wasinger, Alexa M.
    Brey, Robert N.
    Dunleavey, James
    St Croix, Brad
    Bann, James G.

  2. Author Address

    Wichita State Univ, Dept Chem, Wichita, KS 67208 USA.Kinesis Vaccines LLC, Grayslake, IL USA.NCI, Tumor Angiogenesis Unit, NIH, Frederick, MD 21701 USA.
    1. Year: 2018
    2. Date: Nov 6
  2. Journal: Frontiers in oncology
  3. FRONTIERS MEDIA SA,
    1. 8
  5. Type of Article: Review
  6. Article Number: 506
  7. ISSN: 2234-943X
  1. Abstract:

    Recent studies reveal that Seneca Valley Virus (SVV) exploits tumor endothelial marker 8 (TEM8) for cellular entry, the same surface receptor pirated by bacterial-derived anthrax toxin. This observation is particularly significant as SVV is a known oncolytic virus which selectively infects and kills tumor cells, particularly those of neuroendocrine origin. TEM8 is a transmembrane glycoprotein that is preferentially upregulated in some tumor cell and tumor-associated stromal cell populations. Both TEM8 and SVV have been evaluated for targeting of tumors of multiple origins, but the connection between the two was previously unknown. Here, we review currently understood interactions between TEM8 and SVV, anthrax protective antigen (PA), and collagen VI, a native binding partner of TEM8, with an emphasis on potential therapeutic directions moving forward.

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External Sources

  1. View Full Text
  2. DOI: 10.3389/fonc.2018.00506
  3. PMID: 30460197
  4. PMCID: PMC6232524
  5. View record in Web of Science®
  6. WOS: 000449314600002

Library Notes

  1. Fiscal Year: FY2018-2019
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