Vascular endocan (ESM-1) is markedly overexpressed in clear cell renal cell carcinoma

Xavier Leroy1, Sebastien Aubert, Laurent Zini

  • 1Department of Pathology, University Hospital, CHRU & Lille II University, Lille, France. x-leroy@chru-lille.fr

Histopathology
|January 28, 2010
PubMed
Abstract

Insights

Endocan, a molecule linked to blood vessel growth, is significantly elevated in kidney cancer patients. This finding suggests endocan may serve as a biomarker for monitoring kidney cancer progression and response to anti-angiogenic treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Emergence of novel anti-angiogenic therapies for kidney cancer necessitates validated effectiveness parameters.
  • Endocan (endothelial cell-specific molecule-1) is a proteoglycan known to increase with pro-angiogenic factors.

Purpose of the Study:

  • To investigate the expression of endocan in different types of kidney cancer.
  • To evaluate endocan as a potential biomarker for monitoring anti-angiogenic therapy response.

Main Methods:

  • Enzyme-linked immunosorbent assays (ELISA) and immunohistochemistry were used to detect circulating and tissue endocan.
  • Reverse transcriptase-polymerase chain reaction (RT-PCR) quantified endocan gene expression.
  • In vitro studies assessed the effect of sunitinib on endocan release.

Main Results:

  • Endocan was detected in the sera of patients with renal clear cell carcinoma (RCC) and papillary carcinoma (PC).
  • Immunohistochemistry revealed endocan expression in endothelial cells of RCC, with minimal expression in PC.
  • RT-PCR and ELISA confirmed significantly elevated endocan levels in RCC patients compared to controls.
  • Sunitinib treatment inhibited vascular endothelial growth factor-induced endocan release in vitro.

Conclusions:

  • Endocan is overexpressed in patients with renal clear cell carcinoma.
  • Endocan shows potential as a biomarker for kidney cancer follow-up.
  • Endocan may serve as a parameter to monitor therapeutic response to anti-angiogenic drugs.