Positive correlation between sialyl Lewis X expression and pathologic findings in renal cell carcinoma

Tozawa, Keiichi; Okamoto, Takashi; Kawai, Noriyasu; Hashimoto, Yuichi; Hayashi, Yutaro; Kohri, Kenjiro

doi:10.1111/j.1523-1755.2005.00216.x

Cited by 28 publications

(24 citation statements)

References 22 publications

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“…with tumor progression and poor prognosis in renal cell carcinoma (RCC) [29]. E-selectin levels in melanoma cancer correlated with poor survival [30].…”

Section: E-selectin (Elam-1 Endothelial Cell Leukocyte Adhesion Molementioning

confidence: 99%

Endothelial Cell Adhesion Molecules and Cancer Progression

Kobayashi

Boelte²,

Lin³

2007

CMC

214

145

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The role of cell adhesion molecules (CAMs), such as intercellular cell adhesion molecule-1 (ICAM-1), vascular endothelial cell adhesion molecule-1 (VCAM-1), E-selectin, and P-selectin, has been studied extensively in the process of inflammation. These molecules are responsible for recruiting leukocytes onto the vascular endothelium before extravasation to the injured tissues. Some circulating cancer cells have been shown to extravasate to a secondary site using a process similar to inflammatory cells. The most studied ligands for CAMs expressed on cancer cells, sialyl Lewis (a/x) antigens, are shown to be involved in adhesion to endothelial cells by binding to E-selectin. This process, shared by inflammatory cells and cancer cells, may partially explain the link between inflammation and tumorigenesis. Furthermore, this process may elucidate the therapeutic benefit of anti-inflammatory drugs in cancer treatment. The complexity of the tumor microenvironment has been revealed in the past decade. Currently, intense investigation is aimed at various aspects of the tumor microenvironment in addition to the tumor cells themselves. Here, we review the role of CAMs in extravasation of circulating cancer cells, a key step in metastasis.

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“…with tumor progression and poor prognosis in renal cell carcinoma (RCC) [29]. E-selectin levels in melanoma cancer correlated with poor survival [30].…”

Section: E-selectin (Elam-1 Endothelial Cell Leukocyte Adhesion Molementioning

confidence: 99%

Endothelial Cell Adhesion Molecules and Cancer Progression

Kobayashi

Boelte²,

Lin³

2007

CMC

214

145

View full text Add to dashboard Cite

show abstract

“…There is compelling clinical and experimental evidence that overexpression of tetrasaccharides sLe x and sLe a correlates with poor prognosis due to enhanced metastatic phenotype in a number of cancer types, including colon, gastric, prostate, renal, pancreatic, and lung cancer (89, 160–165). Enhanced expression of sLe x/a on cancer cells correlated with increased ability to adhere to E-selectin or to the activated endothelial cells and stromal cells in vitro (157, 166–168).…”

Section: Selectin Ligand Expression Correlates With Cancer Progressionmentioning

confidence: 99%

Altered Tumor-Cell Glycosylation Promotes Metastasis

2014

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Malignant transformation of cells is associated with aberrant glycosylation presented on the cell-surface. Commonly observed changes in glycan structures during malignancy encompass aberrant expression and glycosylation of mucins; abnormal branching of N-glycans; and increased presence of sialic acid on proteins and glycolipids. Accumulating evidence supports the notion that the presence of certain glycan structures correlates with cancer progression by affecting tumor-cell invasiveness, ability to disseminate through the blood circulation and to metastasize in distant organs. During metastasis tumor-cell-derived glycans enable binding to cells in their microenvironment including endothelium and blood constituents through glycan-binding receptors – lectins. In this review, we will discuss current concepts how tumor-cell-derived glycans contribute to metastasis with the focus on three types of lectins: siglecs, galectins, and selectins. Siglecs are present on virtually all hematopoietic cells and usually negatively regulate immune responses. Galectins are mostly expressed by tumor cells and support tumor-cell survival. Selectins are vascular adhesion receptors that promote tumor-cell dissemination. All lectins facilitate interactions within the tumor microenvironment and thereby promote cancer progression. The identification of mechanisms how tumor glycans contribute to metastasis may help to improve diagnosis, prognosis, and aid to develop clinical strategies to prevent metastasis.

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“…Interaction of tumor cell surface sLe x moieties and sLe x -decorated glycoproteins with endothelium E-selectin is a major component of cancer invasion and metastasis. A positive correlation between expression of E-selectin ligands such as sLe x moieties in tumor cells and tumor cell metastasis or invasion has been widely reported [5], [6]. In breast cancer cells, several studies have also demonstrated a critical role for E-selectin in regulating tumor cell transendothelial migration [7], [8].…”

Section: Introductionmentioning

confidence: 99%

CD44v4 Is a Major E-Selectin Ligand that Mediates Breast Cancer Cell Transendothelial Migration

et al. 2008

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BackgroundEndothelial E-selectin has been shown to play a pivotal role in mediating cell–cell interactions between breast cancer cells and endothelial monolayers during tumor cell metastasis. However, the counterreceptor for E-selectin and its role in mediating breast cancer cell transendothelial migration remain unknown.Methodology/Principal FindingsBy assessing migration of various breast cancer cells across TNF-α pre-activated human umbilical vein endothelial cells (HUVECs), we found that breast cancer cells migrated across HUVEC monolayers differentially and that transmigration was E-selectin dependent. Cell surface labeling with the E-selectin extracellular domain/Fc chimera (exE-selectin/Fc) showed that the transmigration capacity of breast cancer cells was correlated to both the expression level and localization pattern of E-selectin binding protein(s) on the tumor cell surface. The exE-selectin/Fc strongly bound to metastatic MDA-MB-231, MDA-MB-435 and MDA-MB-468 cells, but not non-metastatic MCF-7 and T47D cells. Binding of exE-selectin/Fc was abolished by removal of tumor cell surface sialyl lewis x (sLex) moieties. Employing an exE-selectin/Fc affinity column, we further purified the counterreceptor of E-selectin from metastatic breast cancer cells. The N-terminal protein sequence and cDNA sequence identified this E-selectin ligand as a ∼170 kD human CD44 variant 4 (CD44v4). Purified CD44v4 showed a high affinity for E-selectin via sLex moieties and, as expected, MDA-MB-231 cell adhesion to and migration across HUVEC monolayers were significantly reduced by down-regulation of tumor cell CD44v4 via CD44v4-specific siRNA.Conclusions/SignificanceWe demonstrated, for the first time, that breast cancer cell CD44v4 is a major E-selectin ligand in facilitating tumor cell migration across endothelial monolayers. This finding offers new insights into the molecular basis of E-selectin–dependent adhesive interactions that mediate breast cancer cell transendothelial metastasis.

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Positive correlation between sialyl Lewis X expression and pathologic findings in renal cell carcinoma

Cited by 28 publications

References 22 publications

Endothelial Cell Adhesion Molecules and Cancer Progression

Endothelial Cell Adhesion Molecules and Cancer Progression

Altered Tumor-Cell Glycosylation Promotes Metastasis

CD44v4 Is a Major E-Selectin Ligand that Mediates Breast Cancer Cell Transendothelial Migration

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