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Expression of Id proteins is regulated by the Bcl-3 proto-oncogene in prostate cancer.

Ahlqvist, Kristofer LU ; Saamarthy, Karunakar LU ; Syed Khaja, A S ; Bjartell, Anders LU and Massoumi, Ramin LU (2013) In Oncogene 32(12). p.1601-1608
Abstract
B-cell leukemia 3 (Bcl-3) is a member of the inhibitor of κB family, which regulates a wide range of biological processes by functioning as a transcriptional activator or as a repressor of target genes. As high levels of Bcl-3 expression and activation have been detected in different types of human cancer, Bcl-3 has been labeled a proto-oncogene. Our study uncovered a markedly upregulated Bcl-3 expression in human prostate cancer (PCa), where inflammatory cell infiltration was observed. Elevated Bcl-3 expression in PCa was dependent on the proinflammatory cytokine interleukin-6-mediated STAT3 activation. Microarray analyses, using Bcl-3 knockdown in PCa cells, identified the inhibitor of DNA-binding (Id) family of helix-loop-helix proteins... (More)
B-cell leukemia 3 (Bcl-3) is a member of the inhibitor of κB family, which regulates a wide range of biological processes by functioning as a transcriptional activator or as a repressor of target genes. As high levels of Bcl-3 expression and activation have been detected in different types of human cancer, Bcl-3 has been labeled a proto-oncogene. Our study uncovered a markedly upregulated Bcl-3 expression in human prostate cancer (PCa), where inflammatory cell infiltration was observed. Elevated Bcl-3 expression in PCa was dependent on the proinflammatory cytokine interleukin-6-mediated STAT3 activation. Microarray analyses, using Bcl-3 knockdown in PCa cells, identified the inhibitor of DNA-binding (Id) family of helix-loop-helix proteins as potential Bcl-3-regulated genes. Bcl-3 knockdown reduced the abundance of Id-1 and Id-2 proteins and boosted PCa cells to be more receptive to undergoing apoptosis following treatment with anticancer drug. Our data imply that inactivation of Bcl-3 may lead to sensitization of cancer cells to chemotherapeutic drug-induced apoptosis, thus suggesting a potential therapeutic strategy in PCa treatment.Oncogene advance online publication, 14 May 2012; doi:10.1038/onc.2012.175. (Less)
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; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Oncogene
volume
32
issue
12
pages
1601 - 1608
publisher
Nature Publishing Group
external identifiers
  • wos:000316456000013
  • pmid:22580608
  • scopus:84884212418
  • pmid:22580608
ISSN
1476-5594
DOI
10.1038/onc.2012.175
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Molecular Tumour Biology (013017540), Urology (013243400), Department of Translational Medicine (013017500)
id
dc8f4da4-888b-489c-a035-87abca423635 (old id 2608873)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22580608?dopt=Abstract
date added to LUP
2016-04-01 10:21:28
date last changed
2024-02-05 03:04:52
@article{dc8f4da4-888b-489c-a035-87abca423635,
  abstract     = {{B-cell leukemia 3 (Bcl-3) is a member of the inhibitor of κB family, which regulates a wide range of biological processes by functioning as a transcriptional activator or as a repressor of target genes. As high levels of Bcl-3 expression and activation have been detected in different types of human cancer, Bcl-3 has been labeled a proto-oncogene. Our study uncovered a markedly upregulated Bcl-3 expression in human prostate cancer (PCa), where inflammatory cell infiltration was observed. Elevated Bcl-3 expression in PCa was dependent on the proinflammatory cytokine interleukin-6-mediated STAT3 activation. Microarray analyses, using Bcl-3 knockdown in PCa cells, identified the inhibitor of DNA-binding (Id) family of helix-loop-helix proteins as potential Bcl-3-regulated genes. Bcl-3 knockdown reduced the abundance of Id-1 and Id-2 proteins and boosted PCa cells to be more receptive to undergoing apoptosis following treatment with anticancer drug. Our data imply that inactivation of Bcl-3 may lead to sensitization of cancer cells to chemotherapeutic drug-induced apoptosis, thus suggesting a potential therapeutic strategy in PCa treatment.Oncogene advance online publication, 14 May 2012; doi:10.1038/onc.2012.175.}},
  author       = {{Ahlqvist, Kristofer and Saamarthy, Karunakar and Syed Khaja, A S and Bjartell, Anders and Massoumi, Ramin}},
  issn         = {{1476-5594}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{1601--1608}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Oncogene}},
  title        = {{Expression of Id proteins is regulated by the Bcl-3 proto-oncogene in prostate cancer.}},
  url          = {{http://dx.doi.org/10.1038/onc.2012.175}},
  doi          = {{10.1038/onc.2012.175}},
  volume       = {{32}},
  year         = {{2013}},
}