Tumor Suppressor Function of CYLD in Nonmelanoma Skin Cancer.
(2011) In Journal of Skin Cancer 2011.- Abstract
- Ubiquitin and ubiquitin-related proteins posttranslationally modify substrates, and thereby alter the functions of their targets. The ubiquitination process is involved in various physiological responses, and dysregulation of components of the ubiquitin system has been linked to many diseases including skin cancer. The ubiquitin pathways activated among skin cancers are highly diverse and may reflect the various characteristics of the cancer type. Basal cell carcinoma and squamous cell carcinoma, the most common types of human skin cancer, are instances where the involvement of the deubiquitination enzyme CYLD has been recently highlighted. In basal cell carcinoma, the tumor suppressor protein CYLD is repressed at the transcriptional... (More)
- Ubiquitin and ubiquitin-related proteins posttranslationally modify substrates, and thereby alter the functions of their targets. The ubiquitination process is involved in various physiological responses, and dysregulation of components of the ubiquitin system has been linked to many diseases including skin cancer. The ubiquitin pathways activated among skin cancers are highly diverse and may reflect the various characteristics of the cancer type. Basal cell carcinoma and squamous cell carcinoma, the most common types of human skin cancer, are instances where the involvement of the deubiquitination enzyme CYLD has been recently highlighted. In basal cell carcinoma, the tumor suppressor protein CYLD is repressed at the transcriptional levels through hedgehog signaling pathway. Downregulation of CYLD in basal cell carcinoma was also shown to interfere with TrkC expression and signaling, thereby promoting cancer progression. By contrast, the level of CYLD is unchanged in squamous cell carcinoma, instead, catalytic inactivation of CYLD in the skin has been linked to the development of squamous cell carcinoma. This paper will focus on the current knowledge that links CYLD to nonmelanoma skin cancers and will explore recent insights regarding CYLD regulation of NF-κB and hedgehog signaling during the development and progression of these types of human tumors. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2336526
- author
- Masoumi, Katarzyna LU ; Hallgren, Gina LU and Massoumi, Ramin LU
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Skin Cancer
- volume
- 2011
- article number
- 614097
- publisher
- Hindawi Limited
- external identifiers
-
- pmid:22235375
- ISSN
- 2090-2905
- DOI
- 10.1155/2011/614097
- language
- English
- LU publication?
- yes
- id
- 92b94ee0-7e59-438d-a8f0-c16488f02155 (old id 2336526)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22235375?dopt=Abstract
- date added to LUP
- 2016-04-01 10:36:31
- date last changed
- 2018-11-21 19:48:28
@article{92b94ee0-7e59-438d-a8f0-c16488f02155,
abstract = {{Ubiquitin and ubiquitin-related proteins posttranslationally modify substrates, and thereby alter the functions of their targets. The ubiquitination process is involved in various physiological responses, and dysregulation of components of the ubiquitin system has been linked to many diseases including skin cancer. The ubiquitin pathways activated among skin cancers are highly diverse and may reflect the various characteristics of the cancer type. Basal cell carcinoma and squamous cell carcinoma, the most common types of human skin cancer, are instances where the involvement of the deubiquitination enzyme CYLD has been recently highlighted. In basal cell carcinoma, the tumor suppressor protein CYLD is repressed at the transcriptional levels through hedgehog signaling pathway. Downregulation of CYLD in basal cell carcinoma was also shown to interfere with TrkC expression and signaling, thereby promoting cancer progression. By contrast, the level of CYLD is unchanged in squamous cell carcinoma, instead, catalytic inactivation of CYLD in the skin has been linked to the development of squamous cell carcinoma. This paper will focus on the current knowledge that links CYLD to nonmelanoma skin cancers and will explore recent insights regarding CYLD regulation of NF-κB and hedgehog signaling during the development and progression of these types of human tumors.}},
author = {{Masoumi, Katarzyna and Hallgren, Gina and Massoumi, Ramin}},
issn = {{2090-2905}},
language = {{eng}},
publisher = {{Hindawi Limited}},
series = {{Journal of Skin Cancer}},
title = {{Tumor Suppressor Function of CYLD in Nonmelanoma Skin Cancer.}},
url = {{https://lup.lub.lu.se/search/files/1987014/2369668.pdf}},
doi = {{10.1155/2011/614097}},
volume = {{2011}},
year = {{2011}},
}