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Inhibition of tumor angiogenesis and melanoma growth by targeting vascular E-selectin

Zhao-Jun Liu1, Runxia Tian, Yan Li

  • 1Department of Surgery, Miller School of Medicine, University of Miami, Miami, FL 33101, USA.

Annals of Surgery
|July 29, 2011
PubMed
Abstract

Insights

Blocking E-selectin significantly inhibits melanoma growth by preventing endothelial progenitor cell homing and tumor angiogenesis. This finding highlights E-selectin as a promising therapeutic target for melanoma treatment.

Area of Science:

  • Oncology
  • Immunology
  • Vascular Biology

Background:

  • Aggressive melanomas express C-X-C chemokine receptor 4 (CXCR4), interacting with stromal cell-derived factor-1alpha (SDF-1α).
  • The CXCR4-SDF-1α axis is implicated in increasing melanoma invasiveness.
  • SDF-1α upregulates E-selectin on endothelial cells, promoting endothelial progenitor cell (EPC) homing.

Purpose of the Study:

  • To investigate if small interfering ribonucleic acid (siRNA)-mediated E-selectin blockade inhibits melanoma angiogenesis and tumor growth.

Main Methods:

  • Human melanoma cells overexpressing SDF-1α were xenografted into SCID mice.
  • E-selectin knockdown in vivo was achieved using E-selectin siRNA.
  • Tumor angiogenesis, EPC homing, and tumor growth were quantified.

Main Results:

  • Overexpression of SDF-1α increased melanoma cell growth, EPC homing, and tumor angiogenesis.
  • Knockdown of vascular E-selectin significantly inhibited SDF-1α-induced EPC homing and tumor angiogenesis.
  • E-selectin blockade decreased melanoma growth in vivo.

Conclusions:

  • Downregulation of vascular E-selectin profoundly inhibits EPC homing, tumor angiogenesis, and tumor growth in a human melanoma xenograft model.
  • E-selectin blockade may suppress E-selectin-mediated EPC-endothelial cell interactions.
  • E-selectin is identified as a novel therapeutic target for inhibiting melanoma angiogenesis and growth.

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