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Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa

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Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa. / Ng, Yi-Zhen; Pourreyron, Celine; Salas-Alanis, Julio C.; Dayal, Jasbani H. S.; Cepeda-Valdes, Rodrigo; Yan, Wenfei; Wright, Sheila; Chen, Mei; Fine, Jo-David; Hogg, Fiona J.; McGrath, John A.; Murrell, Dedee F.; Leigh, Irene M.; Lane, E. Birgit; South, Andrew P. (Lead / Corresponding author).

In: Cancer Research, Vol. 72, No. 14, 2012, p. 3522-3534.

Research output: Contribution to journalArticle

Harvard

Ng, Y-Z, Pourreyron, C, Salas-Alanis, JC, Dayal, JHS, Cepeda-Valdes, R, Yan, W, Wright, S, Chen, M, Fine, J-D, Hogg, FJ, McGrath, JA, Murrell, DF, Leigh, IM, Lane, EB & South, AP 2012, 'Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa' Cancer Research, vol 72, no. 14, pp. 3522-3534.

APA

Ng, Y-Z., Pourreyron, C., Salas-Alanis, J. C., Dayal, J. H. S., Cepeda-Valdes, R., Yan, W., Wright, S., Chen, M., Fine, J-D., Hogg, F. J., McGrath, J. A., Murrell, D. F., Leigh, I. M., Lane, E. B., & South, A. P. (2012). Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa. Cancer Research, 72(14), 3522-3534doi: 10.1158/0008-5472.CAN-11-2996

Vancouver

Ng Y-Z, Pourreyron C, Salas-Alanis JC, Dayal JHS, Cepeda-Valdes R, Yan W et al. Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa. Cancer Research. 2012;72(14):3522-3534.

Author

Ng, Yi-Zhen; Pourreyron, Celine; Salas-Alanis, Julio C.; Dayal, Jasbani H. S.; Cepeda-Valdes, Rodrigo; Yan, Wenfei; Wright, Sheila; Chen, Mei; Fine, Jo-David; Hogg, Fiona J.; McGrath, John A.; Murrell, Dedee F.; Leigh, Irene M.; Lane, E. Birgit; South, Andrew P. (Lead / Corresponding author) / Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa.

In: Cancer Research, Vol. 72, No. 14, 2012, p. 3522-3534.

Research output: Contribution to journalArticle

Bibtex - Download

@article{97a996e0f5674372a6319ebef2741cf2,
title = "Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa",
author = "Yi-Zhen Ng and Celine Pourreyron and Salas-Alanis, {Julio C.} and Dayal, {Jasbani H. S.} and Rodrigo Cepeda-Valdes and Wenfei Yan and Sheila Wright and Mei Chen and Jo-David Fine and Hogg, {Fiona J.} and McGrath, {John A.} and Murrell, {Dedee F.} and Leigh, {Irene M.} and Lane, {E. Birgit} and South, {Andrew P.}",
year = "2012",
volume = "72",
number = "14",
pages = "3522--3534",
journal = "Cancer Research",
issn = "0008-5472",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Fibroblast-derived dermal matrix drives development of aggressive cutaneous squamous cell carcinoma in patients with recessive dystrophic epidermolysis bullosa

A1 - Ng,Yi-Zhen

A1 - Pourreyron,Celine

A1 - Salas-Alanis,Julio C.

A1 - Dayal,Jasbani H. S.

A1 - Cepeda-Valdes,Rodrigo

A1 - Yan,Wenfei

A1 - Wright,Sheila

A1 - Chen,Mei

A1 - Fine,Jo-David

A1 - Hogg,Fiona J.

A1 - McGrath,John A.

A1 - Murrell,Dedee F.

A1 - Leigh,Irene M.

A1 - Lane,E. Birgit

A1 - South,Andrew P.

AU - Ng,Yi-Zhen

AU - Pourreyron,Celine

AU - Salas-Alanis,Julio C.

AU - Dayal,Jasbani H. S.

AU - Cepeda-Valdes,Rodrigo

AU - Yan,Wenfei

AU - Wright,Sheila

AU - Chen,Mei

AU - Fine,Jo-David

AU - Hogg,Fiona J.

AU - McGrath,John A.

AU - Murrell,Dedee F.

AU - Leigh,Irene M.

AU - Lane,E. Birgit

AU - South,Andrew P.

PY - 2012

Y1 - 2012

N2 - Patients with the genetic skin blistering disease recessive dystrophic epidermolysis bullosa (RDEB) develop aggressive cutaneous squamous cell carcinoma (cSCC). Metastasis leading to mortality is greater in RDEB than in other patient groups with cSCC. Here we investigate the dermal component in RDEB using mRNA expression profiling to compare cultured fibroblasts isolated from individuals without cSCC and directly from tumor matrix in RDEB and non-RDEB samples. Although gene expression of RDEB normal skin fibroblasts resembled that of cancer-associated fibroblasts, RDEB cancer-associated fibroblasts exhibited a distinct and divergent gene expression profile, with a large proportion of the differentially expressed genes involved in matrix and cell adhesion. RDEB cancer-associated fibroblasts conferred increased adhesion and invasion to tumor and non-tumor keratinocytes. Reduction of COL7A1, the defective gene in RDEB, in normal dermal fibroblasts led to increased type XII collagen, thrombospondin-1, and Wnt-5A, while reexpression of wild type COL7A1 in RDEB fibroblasts decreased type XII collagen, thrombospondin-1, and Wnt-5A expression, reduced tumor cell invasion in organotypic culture, and restricted tumor growth in vivo. Overall, our findings show that matrix composition in patients with RDEB is a permissive environment for tumor development, and type VII collagen directly regulates the composition of matrix proteins secreted by dermal and cancer-associated fibroblasts. ©2012 AACR.

AB - Patients with the genetic skin blistering disease recessive dystrophic epidermolysis bullosa (RDEB) develop aggressive cutaneous squamous cell carcinoma (cSCC). Metastasis leading to mortality is greater in RDEB than in other patient groups with cSCC. Here we investigate the dermal component in RDEB using mRNA expression profiling to compare cultured fibroblasts isolated from individuals without cSCC and directly from tumor matrix in RDEB and non-RDEB samples. Although gene expression of RDEB normal skin fibroblasts resembled that of cancer-associated fibroblasts, RDEB cancer-associated fibroblasts exhibited a distinct and divergent gene expression profile, with a large proportion of the differentially expressed genes involved in matrix and cell adhesion. RDEB cancer-associated fibroblasts conferred increased adhesion and invasion to tumor and non-tumor keratinocytes. Reduction of COL7A1, the defective gene in RDEB, in normal dermal fibroblasts led to increased type XII collagen, thrombospondin-1, and Wnt-5A, while reexpression of wild type COL7A1 in RDEB fibroblasts decreased type XII collagen, thrombospondin-1, and Wnt-5A expression, reduced tumor cell invasion in organotypic culture, and restricted tumor growth in vivo. Overall, our findings show that matrix composition in patients with RDEB is a permissive environment for tumor development, and type VII collagen directly regulates the composition of matrix proteins secreted by dermal and cancer-associated fibroblasts. ©2012 AACR.

UR - http://www.scopus.com/inward/record.url?partnerID=yv4JPVwI&eid=2-s2.0-84863914039&md5=ba93f53453796143777e1ee26c9aa54d

U2 - 10.1158/0008-5472.CAN-11-2996

DO - 10.1158/0008-5472.CAN-11-2996

M1 - Article

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 14

VL - 72

SP - 3522

EP - 3534

ER -

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