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Updated: Jul 1, 2025

Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis
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CD93 maintains endothelial barrier function and limits metastatic dissemination.

Kalyani Vemuri1, Beatriz de Alves Pereira1, Patricia Fuenzalida1

  • 1Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.

JCI Insight
|March 5, 2024
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Summary

CD93 protein is crucial for maintaining blood vessel integrity and preventing cancer spread. Its absence in melanoma models increased metastasis, highlighting CD93 as a potential therapeutic target for antiangiogenic therapy.

Keywords:
Endothelial cellsExtracellular matrixMelanomaOncologyVascular biology

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Area of Science:

  • Oncology
  • Vascular Biology
  • Immunology

Background:

  • Compromised vascular integrity is a key driver of cancer cell extravasation and metastatic dissemination.
  • CD93 is a known target for antiangiogenic therapy, but its role in maintaining vascular integrity in metastatic cancers remains unclear.

Purpose of the Study:

  • To investigate the role of CD93 in maintaining endothelial barrier function and its impact on metastatic dissemination in cancer.

Main Methods:

  • Utilized CD93 knockout (CD93-/-) mice and wild-type littermates to study primary melanoma growth and metastasis.
  • Assessed endothelial barrier integrity by examining adherens and tight junctions.
  • Measured matrix metalloprotease 9 (MMP-9) expression at metastatic sites.
  • Investigated the interaction between CD93 and vascular endothelial growth factor receptor 2 (VEGFR2).
  • Administered anti-VEGFR2 antibody therapy to evaluate its effect on vascular integrity and metastasis.

Main Results:

  • CD93-/- mice exhibited increased metastatic dissemination despite hampered primary tumor growth.
  • Absence of CD93 led to disrupted adherens and tight junctions in tumor endothelial cells and elevated MMP-9 expression.
  • CD93 directly interacts with VEGFR2; its absence caused VEGF-induced hyperphosphorylation of VEGFR2.
  • Anti-VEGFR2 antibody therapy restored endothelial barrier function and reduced metastatic burden in CD93-/- mice.

Conclusions:

  • CD93 plays a critical role in maintaining endothelial barrier integrity and suppressing metastatic dissemination.
  • Targeting CD93 or its interaction with VEGFR2 may offer a therapeutic strategy for controlling pathological angiogenesis and metastasis in cancer.