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The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro

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The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro. / Cheung, Belamy B.; Koach, Jessica; Tan, Owen; Kim, Patrick; Bell, Jessica L.; D'andreti, Carla; Sutton, Selina; Malyukova, Alena; Sekyere, Eric; Norris, Murray; Haber, Michelle; Kavallaris, Maria; Cunningham, Anne M.; Proby, Charlotte; Leigh, Irene; Wilmott, James S.; Cooper, Caroline L.; Halliday, Gary M.; Scolyer, Richard A.; Marshall, Glenn M.

In: Journal of Pathology, Vol. 226, No. 3, 02.2012, p. 451-462.

Research output: Contribution to journalArticle

Harvard

Cheung, BB, Koach, J, Tan, O, Kim, P, Bell, JL, D'andreti, C, Sutton, S, Malyukova, A, Sekyere, E, Norris, M, Haber, M, Kavallaris, M, Cunningham, AM, Proby, C, Leigh, I, Wilmott, JS, Cooper, CL, Halliday, GM, Scolyer, RA & Marshall, GM 2012, 'The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro' Journal of Pathology, vol 226, no. 3, pp. 451-462., 10.1002/path.2986

APA

Cheung, B. B., Koach, J., Tan, O., Kim, P., Bell, J. L., D'andreti, C., ... Marshall, G. M. (2012). The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro. Journal of Pathology, 226(3), 451-462. 10.1002/path.2986

Vancouver

Cheung BB, Koach J, Tan O, Kim P, Bell JL, D'andreti C et al. The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro. Journal of Pathology. 2012 Feb;226(3):451-462. Available from: 10.1002/path.2986

Author

Cheung, Belamy B.; Koach, Jessica; Tan, Owen; Kim, Patrick; Bell, Jessica L.; D'andreti, Carla; Sutton, Selina; Malyukova, Alena; Sekyere, Eric; Norris, Murray; Haber, Michelle; Kavallaris, Maria; Cunningham, Anne M.; Proby, Charlotte; Leigh, Irene; Wilmott, James S.; Cooper, Caroline L.; Halliday, Gary M.; Scolyer, Richard A.; Marshall, Glenn M. / The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro.

In: Journal of Pathology, Vol. 226, No. 3, 02.2012, p. 451-462.

Research output: Contribution to journalArticle

Bibtex - Download

@article{ef4a2581ecd247f2be15453d170c447c,
title = "The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro",
keywords = "TRIM16, tripartite motif protein, squamous cell carcinoma, vimentin, E2F1, B-BOX PROTEIN, CHROMOSOME 17P, ACID, ISOTRETINOIN, REGULATOR, E2F-1, LINES, RISK, BETA",
author = "Cheung, {Belamy B.} and Jessica Koach and Owen Tan and Patrick Kim and Bell, {Jessica L.} and Carla D'andreti and Selina Sutton and Alena Malyukova and Eric Sekyere and Murray Norris and Michelle Haber and Maria Kavallaris and Cunningham, {Anne M.} and Charlotte Proby and Irene Leigh and Wilmott, {James S.} and Cooper, {Caroline L.} and Halliday, {Gary M.} and Scolyer, {Richard A.} and Marshall, {Glenn M.}",
year = "2012",
doi = "10.1002/path.2986",
volume = "226",
number = "3",
pages = "451--462",
journal = "Journal of Pathology",
issn = "0022-3417",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro

A1 - Cheung,Belamy B.

A1 - Koach,Jessica

A1 - Tan,Owen

A1 - Kim,Patrick

A1 - Bell,Jessica L.

A1 - D'andreti,Carla

A1 - Sutton,Selina

A1 - Malyukova,Alena

A1 - Sekyere,Eric

A1 - Norris,Murray

A1 - Haber,Michelle

A1 - Kavallaris,Maria

A1 - Cunningham,Anne M.

A1 - Proby,Charlotte

A1 - Leigh,Irene

A1 - Wilmott,James S.

A1 - Cooper,Caroline L.

A1 - Halliday,Gary M.

A1 - Scolyer,Richard A.

A1 - Marshall,Glenn M.

AU - Cheung,Belamy B.

AU - Koach,Jessica

AU - Tan,Owen

AU - Kim,Patrick

AU - Bell,Jessica L.

AU - D'andreti,Carla

AU - Sutton,Selina

AU - Malyukova,Alena

AU - Sekyere,Eric

AU - Norris,Murray

AU - Haber,Michelle

AU - Kavallaris,Maria

AU - Cunningham,Anne M.

AU - Proby,Charlotte

AU - Leigh,Irene

AU - Wilmott,James S.

AU - Cooper,Caroline L.

AU - Halliday,Gary M.

AU - Scolyer,Richard A.

AU - Marshall,Glenn M.

PY - 2012/2

Y1 - 2012/2

N2 - <p>Retinoid therapy is used for chemo-prevention in immuno-suppressed patients at high risk of developing skin cancer. The retinoid signalling molecule, tripartite motif protein 16 (TRIM16), is a regulator of keratinocyte differentiation and a tumour suppressor in retinoid-sensitive neuroblastoma. We sought to determine the role of TRIM16 in skin squamous cell carcinoma (SCC) pathogenesis. We have shown that TRIM16 expression was markedly reduced during the histological progression from normal skin to actinic keratosis and SCC. SCC cell lines exhibited lower cytoplasmic and nuclear TRIM16 expression compared with primary human keratinocyte (PHK) cells due to reduced TRIM16 protein stability. Overexpressed TRIM16 translocated to the nucleus, inducing growth arrest and cell differentiation. In SCC cells, TRIM16 bound to and down regulated nuclear E2F1, this is required for cell replication. Retinoid treatment increased nuclear TRIM16 expression in retinoid-sensitive PHK cells, but not in retinoid-resistant SCC cells. Overexpression of TRIM16 reduced SCC cell migration, which required the C-terminal RET finger protein (RFP)-like domain of TRIM16. The mesenchymal intermediate filament protein, vimentin, was directly bound and down-regulated by TRIM16 and was required for TRIM16-reduced cell migration. Taken together, our data suggest that loss of TRIM16 expression plays an important role in the development of cutaneous SCC and is a determinant of retinoid sensitivity. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.</p>

AB - <p>Retinoid therapy is used for chemo-prevention in immuno-suppressed patients at high risk of developing skin cancer. The retinoid signalling molecule, tripartite motif protein 16 (TRIM16), is a regulator of keratinocyte differentiation and a tumour suppressor in retinoid-sensitive neuroblastoma. We sought to determine the role of TRIM16 in skin squamous cell carcinoma (SCC) pathogenesis. We have shown that TRIM16 expression was markedly reduced during the histological progression from normal skin to actinic keratosis and SCC. SCC cell lines exhibited lower cytoplasmic and nuclear TRIM16 expression compared with primary human keratinocyte (PHK) cells due to reduced TRIM16 protein stability. Overexpressed TRIM16 translocated to the nucleus, inducing growth arrest and cell differentiation. In SCC cells, TRIM16 bound to and down regulated nuclear E2F1, this is required for cell replication. Retinoid treatment increased nuclear TRIM16 expression in retinoid-sensitive PHK cells, but not in retinoid-resistant SCC cells. Overexpression of TRIM16 reduced SCC cell migration, which required the C-terminal RET finger protein (RFP)-like domain of TRIM16. The mesenchymal intermediate filament protein, vimentin, was directly bound and down-regulated by TRIM16 and was required for TRIM16-reduced cell migration. Taken together, our data suggest that loss of TRIM16 expression plays an important role in the development of cutaneous SCC and is a determinant of retinoid sensitivity. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.</p>

KW - TRIM16

KW - tripartite motif protein

KW - squamous cell carcinoma

KW - vimentin

KW - E2F1

KW - B-BOX PROTEIN

KW - CHROMOSOME 17P

KW - ACID

KW - ISOTRETINOIN

KW - REGULATOR

KW - E2F-1

KW - LINES

KW - RISK

KW - BETA

U2 - 10.1002/path.2986

DO - 10.1002/path.2986

M1 - Article

JO - Journal of Pathology

JF - Journal of Pathology

SN - 0022-3417

IS - 3

VL - 226

SP - 451

EP - 462

ER -

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