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Solid tumor therapy by selectively targeting stromal endothelial cells.

Shihui Liu1, Jie Liu2, Qian Ma3

  • 1Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892; shihui.liu@nih.gov sleppla@niaid.nih.gov.

Proceedings of the National Academy of Sciences of the United States of America
|July 1, 2016
PubMed
Summary
This summary is machine-generated.

Engineered anthrax toxins target tumor endothelial cells expressing CMG2, suppressing solid tumor growth in mice. Repeated doses, enabled by immunosuppression, offer a durable antitumor effect for various cancers.

Keywords:
CMG2TEM8angiogenesisanthrax toxintumor targeting

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biotechnology

Background:

  • Engineered anthrax lethal toxin proteins show promise in suppressing solid tumor growth.
  • Toxins utilize tumor endothelium marker-8 and capillary morphogenesis protein-2 (CMG2) receptors, often found on tumor endothelium.
  • Previous studies suggested these receptors are crucial for tumor growth.

Purpose of the Study:

  • To investigate the mechanism of engineered toxin efficacy against solid tumors.
  • To determine the role of CMG2 and tumor endothelium in toxin-mediated tumor suppression.
  • To evaluate the potential for repeated toxin administration for durable antitumor effects.

Main Methods:

  • Utilized tissue-specific loss-of-function and gain-of-function genetic models in mice.
  • Assessed toxin sensitivity of tumor cells in vitro and in vivo.
  • Investigated the role of CMG2 expression on host-derived tumor endothelial cells.
  • Administered an immunosuppressive regimen to allow for multiple toxin dosages.

Main Results:

  • Neither tumor endothelium marker-8 nor CMG2 is required for tumor growth.
  • Tumor cells resistant in vitro become highly sensitive to toxins when implanted in vivo.
  • In vivo toxin sensitivity is dependent on CMG2 expression on host-derived tumor endothelial cells.
  • Engineered toxins suppressed the proliferation of isolated tumor endothelial cells.
  • Multiple toxin dosages, facilitated by immunosuppression, produced a strong and durable antitumor effect.

Conclusions:

  • Engineered anthrax toxins specifically target tumor endothelial cells via CMG2, leading to tumor growth suppression.
  • The in vivo sensitivity of tumor cells is mediated by host endothelial CMG2.
  • A strategy of repeated toxin administration with immunosuppression can achieve durable antitumor effects.
  • This approach holds potential for treating a wide range of solid tumors.