Cited by 114Prostate Cancer Treatment and ResearchNF-κB Signaling PathwaysEstrogen and related hormone effects

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Aberrant activation of the androgen receptor by NF-κB2/p52 in prostate cancer cells.

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Nadiminty, Nagalakshmi, Lou, Wei, Sun, Meng, Chen, Jun, Yue, Jiao, Kung, Hsing-Jien, Evans, Christopher P., Zhou, Qinghua, Gao, Allen C.·2010·Cancer Research

DOI 10.1158/0008-5472.can-09-3703PMC PMC3041633

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Abstract

Prostate cancer initiation and progression are uniquely dependent on the androgen receptor (AR). Even when the cancer progresses to a castration-resistant stage, AR signaling remains active via a variety of mechanisms. In the present study, we showed that NF-kappaB/p52 can activate the AR, resulting in increased transactivation of AR-responsive genes, such as PSA and NKX3.1, in a ligand-independent manner. NF-kappaB2/p52 enhances nuclear translocation and activation of AR by interacting with its NH(2)-terminal domain and enhances the recruitment of coactivators such as p300 to the promoters of AR-dependent genes. These results were confirmed in three different prostate cancer cell lines: LAPC-4 (wild-type AR), LNCaP (mutant AR), and C4-2 (castration resistant). Transfection of p52 into LAPC-4 and LNCaP cells (which express low levels of p52) showed increased activation of the endogenous AR. Downregulation of endogenous p52 in C4-2 cells resulted in abrogation of AR constitutive activation. Comparison of the relative effects of p52 and p65 (RelA) showed that p52, but not p65, could activate the AR. Collectively, these findings, together with previous reports that the levels of NF-kappaB2/p52 are elevated in prostate cancer cells and that active NF-kappaB2/p52 promotes prostate cancer cell growth in vitro and in vivo, suggest that NF-kappaB2/p52 may play a critical role in the progression of castration-resistant prostate cancer.

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1 retracted

RETRACTED: Stat3 enhances the growth of LNCaP human prostate cancer cells in intact and castrated male nude mice
DeMiguel, F., Lee, S. O., Lou, W., Xiao, X., Pflug, B. R., Nelson, J. B., & Gao, A. C. (2002) · The Prostate · doi:10.1002/pros.10110 · Cited by 51
Self-citation
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Self-citation

Authors: Nadiminty, N., Lou, W., Sun, M., Chen, J., Yue, J., Kung, H.-J., Evans, C. P., Zhou, Q., & Gao, A. C.
Affiliations: Tianjin Medical University General Hospital (CN)
Corresponding author: Gao, Allen C.
ORCID: Nadiminty, Nagalakshmi
Lou, Wei
Chen, Jun
Evans, Christopher P.
Zhou, Qinghua
Gao, Allen C.
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2010-04-14
Volume: 70
Issue: 8
Pages: 3309-3319
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-09-3703
PMC: PMC3041633
OpenAlex: W2126127142
Cited by: 113
References: 49
Citations by year: 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 8 · 2021: 3 · 2020: 5 · 2019: 5 · 2018: 10 · 2017: 4 · 2016: 5 · 2015: 9 · 2014: 10 · 2013: 9 · 2012: 7
FWCI: 12.49
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: University of Rochester
National Cancer Institute (CA118887, R01CA118887, CA 109441, R01CA140468, R01CA109441, PC080538)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Keywords: androgen receptor, prostate cancer, castration-resistant prostate cancer, ligand-independent receptor activation, p300 coactivator, RelA/p65, prostate-specific antigen, NKX3.1, transcriptional activation, nuclear translocation
MeSH terms: Src Homology 2 Domain-Containing, Transforming Protein 1, Cell Nucleus, Humans, Male, Models, Biological, Promoter Regions, Genetic, Prostatic Neoplasms, Receptors, Androgen, Transcriptional Activation, Gene Expression Regulation, Neoplastic, NF-kappa B, Protein Structure, Tertiary, Disease Progression, Cell Line, Tumor, p300-CBP Transcription Factors, Shc Signaling Adaptor Proteins

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Aberrant activation of the androgen receptor by NF-κB2/p52 in prostate cancer cells.

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