Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis

Selina K. Sutton; Belamy B. Cheung; Hassina Massudi; Owen Tan; Jessica Koach; Chelsea Mayoh; Daniel R. Carter; Glenn M. Marshall

doi:10.1007/s00432-019-02981-5

Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis

Selina K. Sutton, Belamy B. Cheung^*, Hassina Massudi, Owen Tan, Jessica Koach, Chelsea Mayoh, Daniel R. Carter, Glenn M. Marshall

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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Abstract

Purpose: The tripartite motif (TRIM)16 acts as a tumour suppressor in both squamous cell carcinoma (SCC) and melanoma. TRIM16 is known to be secreted by keratinocytes, but no studies have been reported yet to assess the relationship between TRIM16 keratinocyte expression and melanoma development.

Methods: To study the role of TRIM16 in skin cancer development, we developed a keratinocyte TRIM16-specific knockout mouse model, and used the classical two-stage skin carcinogenesis challenge method, to assess the loss of keratinocyte TRIM16 on both papilloma, SCC and melanoma development in the skin after topical carcinogen treatment.

Results: Heterozygous, but not homozygous, TRIM16 knockout mice exhibited an accelerated development of skin papillomas and melanomas, larger melanoma lesions and an increased potential for lymph node metastasis.

Conclusion: This study provides the first evidence that keratinocyte loss of the putative melanoma tumour suppressor protein, TRIM16, enhances melanomagenesis. Our data also suggest that TRIM16 expression in keratinocytes is involved in cross talk between keratinocytes and melanocytes, and has a role in melanoma tumorigenesis.

Original language	English
Pages (from-to)	2241-2250
Number of pages	10
Journal	Journal of Cancer Research and Clinical Oncology
Volume	145
Issue number	9
DOIs	https://doi.org/10.1007/s00432-019-02981-5
Publication status	Published - 4 Sept 2019
Externally published	Yes

Bibliographical note

Copyright The Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

Carcinogenesis
Keratinocyte
Melanoma
Metastasis
Migration
TRIM16

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Publisher version (open access)Final published version, 1.42 MBLicence: CC BY

Cite this

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title = "Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis",

abstract = "Purpose: The tripartite motif (TRIM)16 acts as a tumour suppressor in both squamous cell carcinoma (SCC) and melanoma. TRIM16 is known to be secreted by keratinocytes, but no studies have been reported yet to assess the relationship between TRIM16 keratinocyte expression and melanoma development.Methods: To study the role of TRIM16 in skin cancer development, we developed a keratinocyte TRIM16-specific knockout mouse model, and used the classical two-stage skin carcinogenesis challenge method, to assess the loss of keratinocyte TRIM16 on both papilloma, SCC and melanoma development in the skin after topical carcinogen treatment.Results: Heterozygous, but not homozygous, TRIM16 knockout mice exhibited an accelerated development of skin papillomas and melanomas, larger melanoma lesions and an increased potential for lymph node metastasis.Conclusion: This study provides the first evidence that keratinocyte loss of the putative melanoma tumour suppressor protein, TRIM16, enhances melanomagenesis. Our data also suggest that TRIM16 expression in keratinocytes is involved in cross talk between keratinocytes and melanocytes, and has a role in melanoma tumorigenesis.",

keywords = "Carcinogenesis, Keratinocyte, Melanoma, Metastasis, Migration, TRIM16",

author = "Sutton, {Selina K.} and Cheung, {Belamy B.} and Hassina Massudi and Owen Tan and Jessica Koach and Chelsea Mayoh and Carter, {Daniel R.} and Marshall, {Glenn M.}",

note = "Copyright The Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.",

year = "2019",

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doi = "10.1007/s00432-019-02981-5",

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T1 - Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis

AU - Sutton, Selina K.

AU - Cheung, Belamy B.

AU - Massudi, Hassina

AU - Tan, Owen

AU - Koach, Jessica

AU - Mayoh, Chelsea

AU - Carter, Daniel R.

AU - Marshall, Glenn M.

N1 - Copyright The Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

PY - 2019/9/4

Y1 - 2019/9/4

N2 - Purpose: The tripartite motif (TRIM)16 acts as a tumour suppressor in both squamous cell carcinoma (SCC) and melanoma. TRIM16 is known to be secreted by keratinocytes, but no studies have been reported yet to assess the relationship between TRIM16 keratinocyte expression and melanoma development.Methods: To study the role of TRIM16 in skin cancer development, we developed a keratinocyte TRIM16-specific knockout mouse model, and used the classical two-stage skin carcinogenesis challenge method, to assess the loss of keratinocyte TRIM16 on both papilloma, SCC and melanoma development in the skin after topical carcinogen treatment.Results: Heterozygous, but not homozygous, TRIM16 knockout mice exhibited an accelerated development of skin papillomas and melanomas, larger melanoma lesions and an increased potential for lymph node metastasis.Conclusion: This study provides the first evidence that keratinocyte loss of the putative melanoma tumour suppressor protein, TRIM16, enhances melanomagenesis. Our data also suggest that TRIM16 expression in keratinocytes is involved in cross talk between keratinocytes and melanocytes, and has a role in melanoma tumorigenesis.

AB - Purpose: The tripartite motif (TRIM)16 acts as a tumour suppressor in both squamous cell carcinoma (SCC) and melanoma. TRIM16 is known to be secreted by keratinocytes, but no studies have been reported yet to assess the relationship between TRIM16 keratinocyte expression and melanoma development.Methods: To study the role of TRIM16 in skin cancer development, we developed a keratinocyte TRIM16-specific knockout mouse model, and used the classical two-stage skin carcinogenesis challenge method, to assess the loss of keratinocyte TRIM16 on both papilloma, SCC and melanoma development in the skin after topical carcinogen treatment.Results: Heterozygous, but not homozygous, TRIM16 knockout mice exhibited an accelerated development of skin papillomas and melanomas, larger melanoma lesions and an increased potential for lymph node metastasis.Conclusion: This study provides the first evidence that keratinocyte loss of the putative melanoma tumour suppressor protein, TRIM16, enhances melanomagenesis. Our data also suggest that TRIM16 expression in keratinocytes is involved in cross talk between keratinocytes and melanocytes, and has a role in melanoma tumorigenesis.

KW - Carcinogenesis

KW - Keratinocyte

KW - Melanoma

KW - Metastasis

KW - Migration

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Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis

Abstract

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