Evidence map›Paper›PMID 23851510›Full record

ArticleOncogene2014

Mechanisms of the androgen receptor splicing in prostate cancer cells.

L L Liu, N Xie, S Sun, S Plymate, E Mostaghel, X Dong

Abstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

208 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. HDAC11 Regulates RNA Splicing via De-Fatty Acylation of SF3B2.bioRxiv : the preprint server for biology · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Increased ErbB2 Signaling Is an Early Adaptation to Androgen Signaling Inhibition and Persists in Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. NXP800 Activates the Unfolded Protein Response, Altering AR and E2F Function to Impact Castration-Resistant Prostate Cancer Growth.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article

148 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

L L LiuDepartment of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
N XieDepartment of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
S SunDepartment of Medicine, University of Washington School of Medicine and VAPSHCS-GRECC, Seattle, WA, USA.
S PlymateDepartment of Medicine, University of Washington School of Medicine and VAPSHCS-GRECC, Seattle, WA, USA.
E MostaghelFred Hutchinson Cancer Research Center, Seattle, WA, USA.
X Dong1] Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada [2] Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario, Canada.

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PETER S NELSON · 2013 to 2026
$25.0M
NCI NIH HHS P01 CA163227NCI NIH HHS P50 CA097186NCI NIH HHS P50CA097186PHS HHS MOP-97934
6 · The paper itself

Abstract

Prostate tumors develop resistance to androgen deprivation therapy (ADT) by multiple mechanisms, one of which is to express constitutively active androgen receptor (AR) splice variants lacking the ligand-binding domain. AR splice variant 7 (AR-V7, also termed AR3) is the most abundantly expressed variant that drives prostate tumor progression under ADT conditions. However, the molecular mechanism by which AR-V7 is generated remains unclear. In this manuscript, we demonstrated that RNA splicing of AR-V7 in response to ADT was closely associated with AR gene transcription initiation and elongation rates. Enhanced AR gene transcription by ADT provides a prerequisite condition that further increases the interactions between AR pre-mRNA and splicing factors. Under ADT conditions, recruitment of several RNA splicing factors to the 3' splicing site for AR-V7 was increased. We identified two RNA splicing enhancers and their binding proteins (U2AF65 and ASF/SF2) that had critical roles in splicing AR pre-mRNA into AR-V7. These data indicate that ADT-induced AR gene transcription rate and splicing factor recruitment to AR pre-mRNA contribute to the enhanced AR-V7 levels in prostate cancer cells.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticAlternative SplicingAndrogensAnimalsApoptosisBlotting, NorthernBlotting, WesternHumansImmunoprecipitationMaleMiceMice, SCIDProstatic NeoplasmsReal-Time Polymerase Chain ReactionReceptors, AndrogenAndrogensAR protein, humanReceptors, AndrogenRNA, Messenger

Identifiers

PMID23851510
PMCPMC4553036

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.