Cited by 81Prostate Cancer Treatment and ResearchEstrogen and related hormone effectsCytokine Signaling Pathways and Interactions

Androgen Receptor Signaling

Jia, Li, Choong, Catherine S-Y., Ricciardelli, Carmela, Kim, Joshua, Tilley, Wayne D., Coetzee, Gerhard A·2004·Cancer Research

Abstract

Nonsteroidal signaling via the androgen receptor (AR) plays an im-portant role in hormone-refractory prostate cancer. Previously, we have reported that the pleiotropic cytokine, interleukin (IL)-6, inhibited dihydrotestosterone-mediated expression of prostate-specific antigen in LNCaP cells (Jia et al., Mol Can Res 2003;1:385-92). In the present study, we explored the mechanisms involved in this inhibition and considered possible effects on AR nuclear translocation, recruitment of transcription cofactors, and the signaling pathways that may mediate this inhibitory effect. IL-6 neither induced nuclear localization of the AR nor inhibited dihydrotestosterone-induced nuclear translocation of the receptor. IL-6 did not affect AR or p160 coactivator recruitment to the transcription initiation complex on the prostate-specific antigen enhancer and promoter. Moreover, it did not lead to the recruitment of the corepressor silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) or histone deacetylase 1 (HDAC1) at the same sites. IL-6 did, however, prevent the recruitment of the secondary coactivator, p300, to the complex and partially inhibited histone H3 acetylation at the same loci. Furthermore, inhibition by IL-6 was not mediated by the mitogen-activated protein kinase or the Akt pathways and was partially abrogated by signal transducers and activators of transcription-3 knock-down using small interfering RNA. Our results show that IL-6 modulates androgen action through the differential recruitment of cofactors to target genes. These findings may account for the pleiotropic actions of IL-6 in malignant prostate cells.

Integrity signals

Registry

Crossref · 10.1158/0008-5472.can-03-3486

Cites

45 of 45 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In the presence of androgen, IL-6 treatment of LNCaP cells impairs transcription of prostate-specific antigen (PSA) via a mechanism that prevents recruitment of the histone acetyltransferase coactivator p300 to the PSA promoter.

    “In the presence of androgen, IL-6 treatment of LNCaP cells impairs transcription of prostate-specific antigen (PSA), via a mechanism that prevents recruitment of the histone acetyltransferase coactivator p300 to the PSA promoter (21).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Jia, L., Choong, C. S.-Y., Ricciardelli, C., Kim, J., Tilley, W. D., & Coetzee, G. A.
Affiliations
  • 1Department of Urology and Preventive Medicine, Norris Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, California, and
  • Hanson Institute (AU)
  • University of Southern California (US)
Venue
Cancer Research
Published
2004-04-01
Volume
64
Issue
7
Pages
2619-2626
ISSN
  • 0008-5472 (ISSN-L)
  • 1538-7445
OpenAlex
W1966572152
Cited by
80
References
45
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 3 · 2018: 1 · 2017: 1 · 2016: 6 · 2014: 4 · 2013: 2 · 2012: 2
FWCI
8.58
Type
journal article
Language
en
Open access
closed
Locations
  • Cancer Research (publishedVersion)
  • PubMed (publishedVersion)
  • Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
Funders
National Cancer Institute (R01CA84890, T32CA009320, R01CA084890)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
androgen receptor, interleukin-6, prostate-specific antigen, castration-resistant prostate cancer, dihydrotestosterone, nuclear translocation, transcriptional coactivator, P300, SMRT, HDAC1, histone H3 acetylation, corepressors, STAT3, MAPK signaling, Akt signaling, LNCaP cells
MeSH terms
Cell Nucleus, DNA-Binding Proteins, Histone Deacetylases, Humans, Male, Nuclear Proteins, Prostatic Neoplasms, Proto-Oncogene Proteins, Receptors, Androgen, Repressor Proteins, Dihydrotestosterone, Signal Transduction, Transcriptional Activation, Trans-Activators, Interleukin-6, Gene Expression, Protein Serine-Threonine Kinases, Prostate-Specific Antigen, Cell Line, Tumor, STAT3 Transcription Factor, Proto-Oncogene Proteins c-akt, Histone Deacetylase 1, Nuclear Receptor Co-Repressor 2

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review