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Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed

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Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed. / Pourreyron, Celine; Reilly, Louise; Proby, Charlotte; Panteleyev, Andrey; Fleming, Colin; McLean, Kathleen; South, Andrew P.; Foerster, John.

In: PLoS ONE, Vol. 7, No. 2, 22.02.2012.

Research output: Contribution to journalArticle

Harvard

Pourreyron, C, Reilly, L, Proby, C, Panteleyev, A, Fleming, C, McLean, K, South, AP & Foerster, J 2012, 'Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed' PLoS ONE, vol 7, no. 2., 10.1371/journal.pone.0031827

APA

Pourreyron, C., Reilly, L., Proby, C., Panteleyev, A., Fleming, C., McLean, K., ... Foerster, J. (2012). Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed. PLoS ONE, 7(2). 10.1371/journal.pone.0031827

Vancouver

Pourreyron C, Reilly L, Proby C, Panteleyev A, Fleming C, McLean K et al. Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed. PLoS ONE. 2012 Feb 22;7(2). Available from: 10.1371/journal.pone.0031827

Author

Pourreyron, Celine; Reilly, Louise; Proby, Charlotte; Panteleyev, Andrey; Fleming, Colin; McLean, Kathleen; South, Andrew P.; Foerster, John / Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed.

In: PLoS ONE, Vol. 7, No. 2, 22.02.2012.

Research output: Contribution to journalArticle

Bibtex - Download

@article{381293469137486ab83c87688d3a78c2,
title = "Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed",
author = "Celine Pourreyron and Louise Reilly and Charlotte Proby and Andrey Panteleyev and Colin Fleming and Kathleen McLean and South, {Andrew P.} and John Foerster",
year = "2012",
doi = "10.1371/journal.pone.0031827",
volume = "7",
number = "2",
journal = "PLoS ONE",
issn = "1932-6203",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressed

A1 - Pourreyron,Celine

A1 - Reilly,Louise

A1 - Proby,Charlotte

A1 - Panteleyev,Andrey

A1 - Fleming,Colin

A1 - McLean,Kathleen

A1 - South,Andrew P.

A1 - Foerster,John

AU - Pourreyron,Celine

AU - Reilly,Louise

AU - Proby,Charlotte

AU - Panteleyev,Andrey

AU - Fleming,Colin

AU - McLean,Kathleen

AU - South,Andrew P.

AU - Foerster,John

PY - 2012/2/22

Y1 - 2012/2/22

N2 - Wnt5a is one of the so-called non-canonical Wnt ligands which do not act through ß-catenin. In normal development, Wnt5a is secreted and directs the migration of target cells along concentration gradients. The effect of Wnt5a on target cells is regulated by many factors, including the expression level of inhibitors and receptors. Dysregulated Wnt5a signalling facilitates invasion of multiple tumor types into adjacent tissue. However, the expression and distribution of Wnt5a in cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), as well as the effect of Wnt5a on keratinocyte migration has not been studied in detail to date. We here report that Wnt5a is upregulated in SCC and BCC and localised to the leading edge of tumors, as well as tumor-associated fibroblasts. The Wnt5a-triggered bundling of its receptor Fzd3 provides evidence of Wnt5a concentration gradients projecting into the tumor. In vitro migration assays show that Wnt5a concentration gradients determine its effect on keratinoctye migration: While chemotactic migration is inhibited by Wnt5a present in homogenous concentrations, it is enhanced in the presence of a Wnt5a gradient. Expression profiling of the Wnt pathway shows that the upregulation of Wnt5a in SCC is coupled to repression of canonical Wnt signalling. This is confirmed by immunohistochemistry showing lack of nuclear ß-catenin, as well as absent accumulation of Axin2. Since both types of Wnt signalling act mutually antogonistically at multiple levels, the concurrent repression of canonical Wnt signalling suggests hyper-active Wnt5a signal transduction. Significantly, this combination of gene dysregulation is not observed in the benign hyperproliferative inflammatory skin disease psoriasis. Collectively, our data strongly suggest that Wnt5a signalling contributes to tissue invasion by non-melanoma skin cancer. © 2012 Pourreyron et al.

AB - Wnt5a is one of the so-called non-canonical Wnt ligands which do not act through ß-catenin. In normal development, Wnt5a is secreted and directs the migration of target cells along concentration gradients. The effect of Wnt5a on target cells is regulated by many factors, including the expression level of inhibitors and receptors. Dysregulated Wnt5a signalling facilitates invasion of multiple tumor types into adjacent tissue. However, the expression and distribution of Wnt5a in cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), as well as the effect of Wnt5a on keratinocyte migration has not been studied in detail to date. We here report that Wnt5a is upregulated in SCC and BCC and localised to the leading edge of tumors, as well as tumor-associated fibroblasts. The Wnt5a-triggered bundling of its receptor Fzd3 provides evidence of Wnt5a concentration gradients projecting into the tumor. In vitro migration assays show that Wnt5a concentration gradients determine its effect on keratinoctye migration: While chemotactic migration is inhibited by Wnt5a present in homogenous concentrations, it is enhanced in the presence of a Wnt5a gradient. Expression profiling of the Wnt pathway shows that the upregulation of Wnt5a in SCC is coupled to repression of canonical Wnt signalling. This is confirmed by immunohistochemistry showing lack of nuclear ß-catenin, as well as absent accumulation of Axin2. Since both types of Wnt signalling act mutually antogonistically at multiple levels, the concurrent repression of canonical Wnt signalling suggests hyper-active Wnt5a signal transduction. Significantly, this combination of gene dysregulation is not observed in the benign hyperproliferative inflammatory skin disease psoriasis. Collectively, our data strongly suggest that Wnt5a signalling contributes to tissue invasion by non-melanoma skin cancer. © 2012 Pourreyron et al.

UR - http://www.scopus.com/inward/record.url?scp=84857486031&partnerID=8YFLogxK

U2 - 10.1371/journal.pone.0031827

DO - 10.1371/journal.pone.0031827

M1 - Article

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 2

VL - 7

ER -

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