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

Leroy, Xavier; Aubert, Sébastien; Zini, Luca; Franquet, Helene; Kervoaze, Gwenola; Villers, Arnauld; Delehedde, Maryse; Copin, Marie‐Christine; Lassalle, Philippe

doi:10.1111/j.1365-2559.2009.03458.x

Cited by 116 publications

(95 citation statements)

References 31 publications

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“…Endocan is a secreted proteoglycan (12) that is upregulated by growth factors and chemokines in vitro (13,14) and on tumor vasculature in several types of cancer (15)(16)(17), with diverse suggested biologic roles (18). Using quantitative reverse-transcription PCR (qRT-PCR) and immunohistochemistry, we found that endocan was strongly upregulated on tumor vascular endothelium and that its expression correlated with the invasiveness of bladder cancer.…”

Section: Introductionmentioning

confidence: 95%

Endocan Is Upregulated on Tumor Vessels in Invasive Bladder Cancer Where It Mediates VEGF-A–Induced Angiogenesis

et al. 2013

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Tumor-associated blood vessels differ from normal vessels and proteins present only on tumor vessels may serve as biomarkers or targets for antiangiogenic therapy in cancer. Comparing the transcriptional profiles of blood vascular endothelium from human invasive bladder cancer with normal bladder tissue, we found that the endothelial cell-specific molecule endocan (ESM1) was highly elevated on tumor vessels. Endocan was associated with filopodia of angiogenic endothelial tip cells in invasive bladder cancer. Notably, endocan expression on tumor vessels correlated strongly with staging and invasiveness, predicting a shorter recurrence-free survival time in noninvasive bladder cancers. Both endocan and VEGF-A levels were higher in plasma of patients with invasive bladder cancer than healthy individuals. Mechanistic investigations in cultured blood vascular endothelial cells or transgenic mice revealed that endocan expression was stimulated by VEGF-A through the phosphorylation and activation of VEGFR-2, which was required to promote cell migration and tube formation by VEGF-A. Taken together, our findings suggest that disrupting endocan interaction with VEGFR-2 or VEGF-A could offer a novel rational strategy to inhibit tumor angiogenesis. Furthermore, they suggest that endocan might serve as a useful biomarker to monitor disease progression and the efficacy of VEGF-A–targeting therapies in patients with bladder cancer. Cancer Res; 73(3); 1097–106. ©2012 AACR.

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Section: Introductionmentioning

confidence: 95%

Endocan Is Upregulated on Tumor Vessels in Invasive Bladder Cancer Where It Mediates VEGF-A–Induced Angiogenesis

et al. 2013

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“…Moreover, in the clear cell renal carcinoma patients (n = 14), endocan levels were significantly higher in pT3-4 tumor stages (n = 8, median value 6.9 ng/ml) than in pT1-2 stages (n = 6, median value 2.0 ng/ ml). However, no significant difference was observed between low (n = 4) and high grade (n = 10) tumors, that could be due of size of the cohort (Leroy et al, 2010).…”

Section: Quantifying Blood Levels Of Endocanmentioning

confidence: 78%

“…The potential of endocan as a prognostic biomarker was also highlighted in a recent study with circulating endocan levels from 3-to 10-fold higher in the sera of clear cell renal carcinoma patients compared to sera from papillary carcinoma patients or from healthy volunteers (Leroy et al, 2010). Moreover, in the clear cell renal carcinoma patients (n = 14), endocan levels were significantly higher in pT3-4 tumor stages (n = 8, median value 6.9 ng/ml) than in pT1-2 stages (n = 6, median value 2.0 ng/ ml).…”

Section: Quantifying Blood Levels Of Endocanmentioning

confidence: 92%

“…Another interesting example on the potential of endocan as a biomarker came over analysis of its expression in tissues issued from renal cancer patients (Leroy et al, 2010). By immunohistochemistry, endocan is detected in the cytoplasm of endothelial cells in clear cell renal carcinoma, decorating each small and large intratumor vessels, but never detected in blood vessels distant from the tumor ( (Huang et al, 2009).…”

Section: Endocan Overexpression In Cancermentioning

confidence: 99%

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Endocan as a Biomarker of Endothelial Dysfunction in Cancer

Sarrazin¹,

Claude-Alain²,

Delmas³

et al. 2010

J Canc Sci Ther

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Endocan also called endothelial cell-specific-molecule-1 is a product of endothelial cells, highly regulated by vascular endothelial growth factor and expressed during the switch between dormant to fast-growing angiogenic tumors. No other molecule is currently known to be a read out of endothelial activation and dysfunction in tumor progression. We here reviewed the present knowledge about endocan that present clinical value as a tissue-and blood-based prognostic and potentially as a companion biomarker in cancer. By immunohistochemistry endocan was shown to be overexpressed into endothelial cells of small and large vessels in lung, kidney and brain tumors. High endocan serum levels were shown to be significantly correlated with the presence of metastasis and with limited survival in kidney and lung cancers. Moreover, endocan release by endothelial cells was in vitro modulated by addition of anti-angiogenic compounds. At a time where biomarkers are hugely needed to improve anti-angiogenic targeted treatments, endocan could be a pertinent biomarker to select patients and/or to clinically monitor the efficacy of cancer drugs. Through its awaited functional applications, endocan appears today as a promising biomarker to access to personalized medicine and to optimize therapy cost / benefit ratio.

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“…IdoA is an important component of the functional structure of endocan. In cancer patients, patients with sepsis and tissue samples of healthy volunteers, serum protein endocan is present in the form of a polysaccharide (1)(2)(3)(4). Studies of the HUVEC vascular endothelial cell model show that the endocan expression level is extremely low, which cannot meet the requirements of scientific research (4).…”

Section: Introductionmentioning

confidence: 99%

Endocan: A new marker for cancer and a target for cancer therapy

Yang

et al. 2015

Biomedical Reports

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Abstract. Endocan, previously known as endothelial cell-specific molecule-1 (ESM-1), was cloned from the human umbilical vein endothelial cell cDNA library. Endocan is a novel ESM, and a 50 kDa soluble proteoglycan. Endocan is secreted into the blood as the soluble proteoglycan, which is the form in the presence of chondroitin sulfate. In normal tissues, chondroitin sulfate/dermatan sulfate proteoglycan is expressed by endothelial cells (such as lung and kidney) and is overexpressed in several carcinoma endothelial cells. There are studies that identified high endocan expression in lung cancer, uterine cancer, kidney cancer, liver cancer, brain glioblastoma, breast cancer and other tumors. Tumor prognosis, metastasis and angiogenesis were shown to be associated with endocan expression. The majority of investigators believe that endocan regulates the tumor by tumor-associated inflammation, angiogenesis, lymphangiogenesis, the tumor cells themselves and other aspects. Endocan may be a new target for cancer therapy.

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

Abstract: Our results showed that endocan is overexpressed in patients with RCC. Endocan could therefore appear as a marker of interest in the follow-up and may be a potential parameter to monitor the tumour response to anti-angiogenic therapeutics.

Cited by 116 publications

References 31 publications

Endocan Is Upregulated on Tumor Vessels in Invasive Bladder Cancer Where It Mediates VEGF-A–Induced Angiogenesis

Endocan Is Upregulated on Tumor Vessels in Invasive Bladder Cancer Where It Mediates VEGF-A–Induced Angiogenesis

Endocan as a Biomarker of Endothelial Dysfunction in Cancer

Endocan: A new marker for cancer and a target for cancer therapy

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