Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

GLI1-dependent transcriptional repression of CYLD in basal cell carcinoma

Kuphal, S. ; Shaw-Hallgren, G. ; Eberl, M. ; Karrer, S. ; Aberger, F. ; Bosserhoff, A. K. and Massoumi, Ramin LU (2011) In Oncogene 30(44). p.4523-4530
Abstract
CYLD is a deubiquitination enzyme that regulates different cellular processes, such as cell proliferation and cell survival. Mutation and loss of heterozygosity of the CYLD gene causes development of cylindromatosis, a benign tumour originating from the skin. Our study shows that CYLD expression is dramatically downregulated in basal cell carcinoma (BCC), the most common cancer in humans. Reduced CYLD expression in basal cell carcinoma was mediated by GLI1-dependent activation of the transcriptional repressor Snail. Inhibition of GLI1 restored the CYLD expression-mediated Snail signaling pathway, and caused a significant delay in the G1 to S phase transition, as well as proliferation. Our data suggest that GLI1-mediated suppression of CYLD... (More)
CYLD is a deubiquitination enzyme that regulates different cellular processes, such as cell proliferation and cell survival. Mutation and loss of heterozygosity of the CYLD gene causes development of cylindromatosis, a benign tumour originating from the skin. Our study shows that CYLD expression is dramatically downregulated in basal cell carcinoma (BCC), the most common cancer in humans. Reduced CYLD expression in basal cell carcinoma was mediated by GLI1-dependent activation of the transcriptional repressor Snail. Inhibition of GLI1 restored the CYLD expression-mediated Snail signaling pathway, and caused a significant delay in the G1 to S phase transition, as well as proliferation. Our data suggest that GLI1-mediated suppression of CYLD has a significant role in basal cell carcinoma progression. Oncogene (2011) 30, 4523-4530; doi: 10.1038/onc.2011.163; published online 16 May 2011 (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
CYLD, GLI1, Snail1, BCC, Bcl-3
in
Oncogene
volume
30
issue
44
pages
4523 - 4530
publisher
Nature Publishing Group
external identifiers
  • wos:000296733200007
  • scopus:80455174799
  • pmid:21577203
ISSN
1476-5594
DOI
10.1038/onc.2011.163
language
English
LU publication?
yes
id
94e5f755-0352-464d-9bea-6826aba25972 (old id 2254144)
date added to LUP
2016-04-01 10:06:04
date last changed
2020-11-22 05:37:28
@article{94e5f755-0352-464d-9bea-6826aba25972,
  abstract     = {CYLD is a deubiquitination enzyme that regulates different cellular processes, such as cell proliferation and cell survival. Mutation and loss of heterozygosity of the CYLD gene causes development of cylindromatosis, a benign tumour originating from the skin. Our study shows that CYLD expression is dramatically downregulated in basal cell carcinoma (BCC), the most common cancer in humans. Reduced CYLD expression in basal cell carcinoma was mediated by GLI1-dependent activation of the transcriptional repressor Snail. Inhibition of GLI1 restored the CYLD expression-mediated Snail signaling pathway, and caused a significant delay in the G1 to S phase transition, as well as proliferation. Our data suggest that GLI1-mediated suppression of CYLD has a significant role in basal cell carcinoma progression. Oncogene (2011) 30, 4523-4530; doi: 10.1038/onc.2011.163; published online 16 May 2011},
  author       = {Kuphal, S. and Shaw-Hallgren, G. and Eberl, M. and Karrer, S. and Aberger, F. and Bosserhoff, A. K. and Massoumi, Ramin},
  issn         = {1476-5594},
  language     = {eng},
  number       = {44},
  pages        = {4523--4530},
  publisher    = {Nature Publishing Group},
  series       = {Oncogene},
  title        = {GLI1-dependent transcriptional repression of CYLD in basal cell carcinoma},
  url          = {http://dx.doi.org/10.1038/onc.2011.163},
  doi          = {10.1038/onc.2011.163},
  volume       = {30},
  year         = {2011},
}