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Quantitative Approaches for Scoring in vivo Neuronal Aggregate and Organelle Extrusion in Large Exopher Vesicles in C. elegans
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Semaphorin 3E, an exception to the rule.

Michael Klagsbrun1, Akio Shimizu

  • 1Department of Surgery, Children's Hospital Boston, and Harvard Medical School, Boston, Massachusetts 02115, USA. michael.klagsbrun@childrens.harvard.edu

The Journal of Clinical Investigation
|July 29, 2010
PubMed
Summary

Class 3 semaphorins (Sema3s) typically inhibit tumor metastasis. However, this study reveals Sema3E paradoxically promotes tumor invasiveness and metastasis, independent of neuropilins but dependent on Plexin D1.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Class 3 semaphorins (Sema3s) are known regulators of axon guidance, angiogenesis, and tumor progression.
  • Neuropilins (NRPs) serve as cell surface receptors for Sema3s, with plexins being essential for signal transduction.
  • Conventional understanding posits Sema3s as inhibitors of tumor metastasis.

Purpose of the Study:

  • To investigate the role of Sema3E in tumor metastasis, challenging the established inhibitory function of Sema3s.
  • To elucidate the molecular mechanisms underlying Sema3E-mediated tumor invasiveness and metastasis.

Main Methods:

  • Analysis of Sema3E's effect on tumor growth, invasiveness, and metastasis in experimental models.
  • Assessment of the dependency of Sema3E's pro-metastatic function on Neuropilin (NRP) and Plexin D1 expression.

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  • Examination of Sema3E and Plexin D1 expression levels in human cancer tissues.

    • Main Results:

    • Sema3E inhibited tumor growth but significantly promoted tumor invasiveness and metastasis.
    • The pro-metastatic effect of Sema3E was found to be dependent on Plexin D1 expression.
    • This metastatic potential was independent of NRP expression.
    • Sema3E and Plexin D1 were observed to be upregulated in human colon cancer, liver metastasis, and melanoma progression.

    Conclusions:

    • Sema3E exhibits an atypical role in tumor metastasis, promoting invasiveness and spread.
    • Plexin D1 is a critical mediator of Sema3E's pro-metastatic function.
    • The upregulation of Sema3E and Plexin D1 in human cancers suggests their potential as therapeutic targets.