Expression of Id proteins is regulated by the Bcl-3 proto-oncogene in prostate cancer.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2608873
- author
- Ahlqvist, Kristofer LU ; Saamarthy, Karunakar LU ; Syed Khaja, A S ; Bjartell, Anders LU and Massoumi, Ramin LU
- organization
- publishing date
- 2013
- 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}}, }