Evidence map›Paper›PMID 21765461›Full record

ArticleOncogene2012

A novel nuclear role for the Vav3 nucleotide exchange factor in androgen receptor coactivation in prostate cancer.

S Rao, L S Lyons, C D Fahrenholtz, F Wu, A Farooq, W Balkan, K L Burnstein

Abstract read
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Rac GTPases in Hematological Malignancies.International journal of molecular sciences · 2018
    Review
  15. Evaluation of Vav3.1 as prognostic marker in endometrial cancer.Journal of cancer research and clinical oncology · 2018
    Article
  16. Review
  17. Article
  18. Review
  19. Review
  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

7 authors at 2 institutions in 1 country.

S RaoDepartment of Molecular and Cellular Pharmacology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
L S Lyons
C D Fahrenholtz
F Wu
A Farooq
W Balkan
K L Burnstein
University of Miami · USNova Southeastern University · US

Funding

TRAINING PROGRAMS IN CARDIOVASCULAR PHARMACOLOGYT32HL007188 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SZCZESNA-CORDARY, DANUTA · 1985 to 2011
$3.8M
Structural and Functional Studies of the Novel DBD Domain of MKP5R01GM083897 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FAROOQ, AMJAD · 2008 to 2012
$1.6M
Vav3 Oncogene Potentiation of Androgen Receptor Signaling in Prostate Cancer.R01CA132200 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BURNSTEIN, KERRY L · 2009 to 2013
$1.6M
NCI NIH HHS R01 CA132200NCI NIH HHS R01CA132200NHLBI NIH HHS T32 HL007188NHLBI NIH HHS T32-HL007188NIGMS NIH HHS R01 GM083897NIGMS NIH HHS R01GM083897
6 · The paper itself

Abstract

Increased androgen receptor (AR) transcriptional activity mediated by coactivator proteins may drive castration-resistant prostate cancer (CRPC) growth. Vav3, a Rho GTPase guanine nucleotide exchange factor (GEF), is overexpressed in human prostate cancers, particularly in models of CRPC progression. Vav3 coactivates AR in a Vav3 pleckstrin homology (PH) domain-dependent but GEF-independent manner. Ectopic expression of Vav3 in androgen-dependent human prostate cancer cells conferred robust castration-resistant xenograft tumor growth. Vav3 but not a Vav3 PH mutant greatly stimulated interaction between the AR amino and carboxyl termini (N-C interaction), which is required for maximal receptor transcriptional activity. Vav3 was distributed between the cytoplasm and nucleus with nuclear localization-dependent on the Vav3 PH domain. Membrane targeting of Vav3 abolished Vav3 potentiation of AR activity, whereas nuclear targeting of a Vav3 PH mutant rescued AR coactivation, suggesting that nuclear localization is an important function of the Vav3 PH domain. A nuclear role for Vav3 was further demonstrated by sequential chromatin immunoprecipitation assays, which revealed that Vav3 and AR were recruited to the same transcriptional complexes of an AR target gene enhancer. These data demonstrate the importance of Vav3 in CRPC and define a novel nuclear function of Vav3 in regulating AR activity.

Indexed as

AnimalsBinding SitesBlotting, WesternCell Line, TumorCell NucleusChromatin ImmunoprecipitationCytoplasmGreen Fluorescent ProteinsHumansMaleMetriboloneMiceMice, SCIDMicroscopy, FluorescenceMutationOrchiectomyGreen Fluorescent ProteinsMetriboloneProto-Oncogene Proteins c-vavReceptors, AndrogenTrans-ActivatorsVAV3 protein, human

Identifiers

PMID21765461
PMCPMC3203328
OpenAlexW1985937576

What OpenQuestion holds

Textmetadata
LicenceTDM
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.