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In vitro analysis of the melanoma/endothelium interaction increasing the release of soluble intercellular adhesion

E Fonsatti1, E Lamaj, S Coral

  • 1Advanced Immunotherapy Unit, Centro di Riferimento Oncologico, I.N.R.C.C.S., Aviano, Italy.

Insights

Soluble intercellular adhesion molecule 1 (sICAM-1) levels in melanoma patients vary. Melanoma-secreted interleukin-1alpha (IL-1alpha) can increase sICAM-1 shedding by endothelial cells, impacting tumor progression.

Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Melanoma cells release soluble intercellular adhesion molecule 1 (sICAM-1), with elevated levels correlating to disease progression.
  • The correlation between sICAM-1 levels and melanoma progression is not absolute, suggesting other factors influence circulating sICAM-1.

Purpose of the Study:

  • To investigate the relationship between sICAM-1 release by metastatic melanomas and ICAM-1 expression on neoplastic cells.
  • To determine the role of melanoma-secreted factors, specifically interleukin-1alpha (IL-1alpha) and vascular endothelial growth factor (VEGF), in regulating sICAM-1 shedding by endothelial cells.
  • To understand how melanoma-derived sICAM-1 and IL-1alpha secretion influence tumor progression and the efficacy of cell-based therapies.

Main Methods:

  • Analysis of sICAM-1 release from 40 metastatic melanoma samples (36 primary cultures, 4 cell lines).
  • Assessment of the correlation between sICAM-1 release and ICAM-1 expression on melanoma cells.
  • Incubation of human umbilical vein endothelial cells (HUVEC) with melanoma-secreted IL-1alpha and VEGF to measure sICAM-1 shedding.
  • Utilized IL-1alpha/beta neutralizing antibodies to assess their impact on sICAM-1 shedding at protein and mRNA levels.

Main Results:

  • A weak correlation (r = 0.55) was observed between sICAM-1 release by melanomas and ICAM-1 expression on neoplastic cells.
  • Melanoma-secreted IL-1alpha, but not VEGF, significantly upregulated sICAM-1 shedding by HUVEC.
  • The IL-1alpha-induced sICAM-1 shedding was abolished by neutralizing antibodies, confirming IL-1alpha's role.
  • VEGF secreted by melanoma cells did not affect ICAM-1 expression or sICAM-1 release by HUVEC.

Conclusions:

  • Individual melanomas exhibit distinct sICAM-1 release patterns, potentially independent of their ICAM-1 expression.
  • Tumor endothelial cells may contribute to sICAM-1 levels in certain melanoma cases through IL-1alpha signaling.
  • Melanoma-derived VEGF does not influence ICAM-1 expression or sICAM-1 shedding by endothelial cells.
  • Constitutive sICAM-1 release and IL-1alpha secretion by melanomas can differentially impact tumor progression and the effectiveness of cytotoxic cell-based vaccines.

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