Evidence map›Paper›PMID 18079321›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

Ligand-independent activation of androgen receptors by Rho GTPase signaling in prostate cancer.

Leah S Lyons, Shuyun Rao, Wayne Balkan, Joanne Faysal, Carol A Maiorino, Kerry L Burnstein

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025
    Article
  6. Review
  7. RISING STARS: Androgens and immune cell function.The Journal of endocrinology · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Inhibition of Vav3 gene can promote apoptosis of human gastric cancer cell line MGC803 by regulating ERK pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  20. Pathway Analysis of Genome-wide Association Study in Childhood Leukemia among Hispanics.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016
    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

6 authors at 2 institutions in 1 country.

Leah S LyonsDepartment of Molecular and Cellular Pharmacology, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.
Shuyun Rao
Wayne Balkan
Joanne Faysal
Carol A Maiorino
Kerry L Burnstein
Geriatric Research Education and Clinical Center · USUniversity of Miami · US

Funding

Vav3, a Rho GEF, Stimulates AR Activity and CaP GrowthR21DK065281 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BURNSTEIN, KERRY L. · 2003 to 2004
$299k
NIDDK NIH HHS DK065281NIDDK NIH HHS R21 DK065281
6 · The paper itself

Abstract

Prostate cancer invariably recurs after androgen deprivation therapy. Growth of this recurrent/androgen-independent form of prostate cancer may be due to increased androgen receptor (AR) transcriptional activity in the absence of androgen. This ligand-independent AR activation is promoted by some growth factors but the mechanism is not well understood. Vav3, a Rho guanosine triphosphatase guanine nucleotide exchange factor, which is activated by growth factors, is up-regulated in human prostate cancer. We show here that Vav3 levels increase during in vivo progression of prostate cancer to androgen independence. Vav3 strikingly enhanced growth factor activation of AR in the absence of androgen. Because Vav3 may be chronically activated in prostate cancer by growth factor receptors, we examined the effects of a constitutively active (Ca) form of Vav3 on AR transcriptional activity. Ca Vav3 caused nuclear localization and ligand-independent activation of AR via the Rho guanosine triphosphatase, Rac1. Ca Rac1 activation of AR occurred, in part, through MAPK/ERK signaling. Expression of active Rac1 conferred androgen-independent growth of prostate cancer cells in culture, soft agar, and mice. These findings suggest that Vav3/Rac 1 signaling is an important modulator of ligand-independent AR transcriptional activity in prostate cancer progression.

Indexed as

AnimalsCell Line, TumorGuanine Nucleotide Exchange FactorsHumansMaleMAP Kinase Signaling SystemMiceMice, NudeMitogen-Activated Protein KinasesNeoplasms, Hormone-DependentNeoplasm TransplantationProstatic NeoplasmsProto-Oncogene Proteins c-vavrac1 GTP-Binding ProteinReceptors, AndrogenReverse Transcriptase Polymerase Chain ReactionAR protein, humanGuanine Nucleotide Exchange FactorsMitogen-Activated Protein KinasesProto-Oncogene Proteins c-vavrac1 GTP-Binding ProteinRAC1 protein, humanReceptors, AndrogenRNA, MessengerVAV3 protein, human

Identifiers

PMID18079321
PMCPMC2262175
OpenAlexW2085254603

What OpenQuestion holds

Textmetadata
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.