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The use of Shiga-like toxin 1 in cancer therapy

J Gariépy1

  • 1Department of Medical Biophysics, University of Toronto, University Health Network, 610 University Ave., Toronto, Ont., Canada, M5G 2M9. gariepy@oci.utoronto.ca

Critical Reviews in Oncology/Hematology
|June 22, 2001
PubMed

Insights

Shiga-like toxin-1 (SLT-1) targets cancer cells expressing CD77 receptors. This toxin shows potential for purging cancer cells from stem cell transplants and treating brain tumors like astrocytoma.

Area of Science:

  • Biochemistry
  • Oncology
  • Immunology

Background:

  • Shiga-like toxin-1 (SLT-1) is a ribosome-inactivating protein.
  • SLT-1 specifically binds to globotriaosylceramide (CD77) receptors on cell surfaces.
  • CD77 receptors are frequently found on various cancer cells but not on healthy hematopoietic stem cells.

Purpose of the Study:

  • To explore the therapeutic potential of SLT-1 in cancer treatment.
  • To evaluate SLT-1 for purging cancer cells from autologous stem cell transplants.
  • To investigate SLT-1's efficacy against specific cancer types, including astrocytoma.

Main Methods:

  • Identifying cancer cell lines expressing CD77 receptors.
  • Assessing the sensitivity of tumor cells to SLT-1.
  • Evaluating the absence of SLT-1 receptors on healthy stem cells for purging applications.
  • Considering in vivo applications for brain tumor treatment.

Main Results:

  • SLT-1 effectively targets CD77-expressing cells, including those from hematological cancers (follicular lymphoma, multiple myeloma, chronic lymphocytic leukemia), breast cancer, ovarian cancer, and astrocytoma.
  • SLT-1 demonstrated high sensitivity against astrocytoma cell lines.
  • SLT-1 receptors were notably absent on human CD34(+) hematopoietic stem cells, indicating a potential for selective purging.

Conclusions:

  • SLT-1 holds promise for ex vivo purging of CD77(+) tumor cells from autologous stem cell transplants.
  • SLT-1 presents a viable therapeutic option for in vivo treatment of astrocytoma and potentially other CD77-expressing cancers.
  • Structural modifications of SLT-1 could broaden its applicability to CD77(-) tumor populations.

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