Evidence map›Paper›PMID 24737870›Full record

ArticleEMBO molecular medicine2014

HES6 drives a critical AR transcriptional programme to induce castration-resistant prostate cancer through activation of an E2F1-mediated cell cycle network.

Antonio Ramos-Montoya, Alastair D Lamb, Roslin Russell, Thomas Carroll, Sarah Jurmeister, Nuria Galeano-Dalmau, Charlie E Massie, Joan Boren, Helene Bon, Vasiliki Theodorou and 11 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.8field-weighted citation impact, top 4% of its field
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

58 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. DNA G-Quadruplex in NRP1 Promoter Facilitates SARS-CoV-2 Infection.International journal of molecular sciences · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. TRAF4-mediated nonproteolytic ubiquitination of androgen receptor promotes castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article
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

21 authors at 5 institutions in 2 countries.

Antonio Ramos-MontoyaUro-Oncology Research Group Cancer Research UK Cambridge Institute University of Cambridge Li Ka Shing Centre, Cambridge, UK.
Alastair D Lamb
Roslin Russell
Thomas Carroll
Sarah Jurmeister
Nuria Galeano-Dalmau
Charlie E Massie
Joan Boren
Helene Bon
Vasiliki Theodorou
Maria Vias
Greg L Shaw
Naomi L Sharma
Helen Ross-Adams
Helen E Scott
Sarah L Vowler
William J Howat
Anne Y Warren
Richard F Wooster
Ian G Mills
David E Neal
University of Cambridge · GBCancer Research UK Cambridge Center · GBAddenbrooke's Hospital · GBCancer Research UK · GBOslo University Hospital · NO

Funding

Cancer Research UKMedical Research Council G0500966Medical Research Council G0900871
6 · The paper itself

Abstract

Castrate-resistant prostate cancer (CRPC) is poorly characterized and heterogeneous and while the androgen receptor (AR) is of singular importance, other factors such as c-Myc and the E2F family also play a role in later stage disease. HES6 is a transcription co-factor associated with stem cell characteristics in neural tissue. Here we show that HES6 is up-regulated in aggressive human prostate cancer and drives castration-resistant tumour growth in the absence of ligand binding by enhancing the transcriptional activity of the AR, which is preferentially directed to a regulatory network enriched for transcription factors such as E2F1. In the clinical setting, we have uncovered a HES6-associated signature that predicts poor outcome in prostate cancer, which can be pharmacologically targeted by inhibition of PLK1 with restoration of sensitivity to castration. We have therefore shown for the first time the critical role of HES6 in the development of CRPC and identified its potential in patient-specific therapeutic strategies.

Indexed as

Gene Expression RegulationAnimalsBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsDisease Models, AnimalE2F1 Transcription FactorGene Expression ProfilingHumansMaleMiceMolecular Sequence DataProstatic NeoplasmsReceptors, AndrogenRepressor ProteinsSequence Analysis, DNAAR protein, humanBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsE2F1 protein, humanE2F1 Transcription FactorHES6 protein, humanReceptors, AndrogenRepressor Proteins

Identifiers

PMID24737870
PMCPMC4023887
OpenAlexW2135254264

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.