Altered tumor cell glycosylation promotes metastasis

Malignant transformation of cells is associated with aberrant glycosylation presented on the cell-surface. Commonly observed changes in glycan structures during malignancy encompasses aberrant expression and glycosylation of mucins; abnormal branching of N-glycans; and increased presence of sialic a...

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Main Authors: Irina eHäuselmann, Lubor eBorsig
Formato: Artigo
Idioma:English
Publicado em: Frontiers Media S.A. 2014-02-01
Colecção:Frontiers in Oncology
Assuntos:
Acesso em linha:http://journal.frontiersin.org/Journal/10.3389/fonc.2014.00028/full
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author Irina eHäuselmann
Lubor eBorsig
author_facet Irina eHäuselmann
Lubor eBorsig
author_sort Irina eHäuselmann
collection DOAJ
description Malignant transformation of cells is associated with aberrant glycosylation presented on the cell-surface. Commonly observed changes in glycan structures during malignancy encompasses 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 hematopoetic 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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spelling doaj.art-2f6b1bccd6614cdb88e5bfb096e1dfb92022-12-22T00:54:46ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2014-02-01410.3389/fonc.2014.0002878416Altered tumor cell glycosylation promotes metastasisIrina eHäuselmann0Lubor eBorsig1Institute of Physiology, University of ZurichInstitute of Physiology, University of ZurichMalignant transformation of cells is associated with aberrant glycosylation presented on the cell-surface. Commonly observed changes in glycan structures during malignancy encompasses 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 hematopoetic 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.http://journal.frontiersin.org/Journal/10.3389/fonc.2014.00028/fullGalectinsGlycosylationMucinsSelectinsCancermetastasis
spellingShingle Irina eHäuselmann
Lubor eBorsig
Altered tumor cell glycosylation promotes metastasis
Frontiers in Oncology
Galectins
Glycosylation
Mucins
Selectins
Cancer
metastasis
title Altered tumor cell glycosylation promotes metastasis
title_full Altered tumor cell glycosylation promotes metastasis
title_fullStr Altered tumor cell glycosylation promotes metastasis
title_full_unstemmed Altered tumor cell glycosylation promotes metastasis
title_short Altered tumor cell glycosylation promotes metastasis
title_sort altered tumor cell glycosylation promotes metastasis
topic Galectins
Glycosylation
Mucins
Selectins
Cancer
metastasis
url http://journal.frontiersin.org/Journal/10.3389/fonc.2014.00028/full
work_keys_str_mv AT irinaehauselmann alteredtumorcellglycosylationpromotesmetastasis
AT luboreborsig alteredtumorcellglycosylationpromotesmetastasis