Evidence map›Paper›PMID 22172722›Full record

ArticleCancer cell2011

WT1 mutants reveal SRPK1 to be a downstream angiogenesis target by altering VEGF splicing.

Elianna M Amin, Sebastian Oltean, Jing Hua, Melissa V R Gammons, Maryam Hamdollah-Zadeh, Gavin I Welsh, Man-Kim Cheung, Lan Ni, Satoru Kase, Emma S Rennel and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

160 citing papers in PubMed, 1 synthesis or guideline pooled it, 246 citations in OpenAlex.

  1. La Tunisie medicale · 2024
    Pooled it
  2. Article
  3. RNA splicing in health and disease.Molecular biomedicine · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. SRPKs: a promising therapeutic target in cancer.Clinical and experimental medicine · 2023
    Review
  18. Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 7 institutions in 4 countries.

Elianna M AminCentre for Research in Biomedicine, University of the West of England, Bristol, UK.
Sebastian Oltean
Jing Hua
Melissa V R Gammons
Maryam Hamdollah-Zadeh
Gavin I Welsh
Man-Kim Cheung
Lan Ni
Satoru Kase
Emma S Rennel
Kirsty E Symonds
Dawid G Nowak
Brigitte Royer-Pokora
Moin A Saleem
Masatoshi Hagiwara
Valérie A Schumacher
Steven J Harper
David R Hinton
David O Bates
Michael R Ladomery
University of Bristol · GBSouthmead Hospital · GBUniversity of Southern California · USUniversity of the West of England · GBBoston Children's Hospital · USHeinrich Heine University Düsseldorf · DEKyoto University · JP

Funding

VISION RESEARCHP30EY003040 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 1985 to 2013
$7.0M
British Heart Foundation BS/06/005/20340British Heart Foundation FS06/003British Heart Foundation PG08/022/21636British Heart Foundation PG/08/054/25272British Heart Foundation PG/11/20/28792Cancer Research UK A5730Cancer Research UK A8451Cancer Research UK C11392/A10484Cancer Research UK CF11392/A8451Medical Research Council G0600920Medical Research Council G0600920(78877)Medical Research Council G10002073Medical Research Council GR0600920NEI NIH HHS EY03040NEI NIH HHS P30 EY003040Wellcome Trust 079736Worldwide Cancer Research 07-0605
6 · The paper itself

Abstract

Angiogenesis is regulated by the balance of proangiogenic VEGF(165) and antiangiogenic VEGF(165)b splice isoforms. Mutations in WT1, the Wilms' tumor suppressor gene, suppress VEGF(165)b and cause abnormal gonadogenesis, renal failure, and Wilms' tumors. In WT1 mutant cells, reduced VEGF(165)b was due to lack of WT1-mediated transcriptional repression of the splicing-factor kinase SRPK1. WT1 bound to the SRPK1 promoter, and repressed expression through a specific WT1 binding site. In WT1 mutant cells SRPK1-mediated hyperphosphorylation of the oncogenic RNA binding protein SRSF1 regulated splicing of VEGF and rendered WT1 mutant cells proangiogenic. Altered VEGF splicing was reversed by wild-type WT1, knockdown of SRSF1, or SRPK1 and inhibition of SRPK1, which prevented in vitro and in vivo angiogenesis and associated tumor growth.

Indexed as

AnimalsCell Line, TumorCell NucleusChoroidal NeovascularizationDenys-Drash SyndromeGene ExpressionGene Expression Regulation, NeoplasticGenes, ReporterHumansLuciferases, RenillaMiceMice, Inbred C57BLMice, NudeNeoplasmsNeoplasm TransplantationNeovascularization, PathologicLuciferases, RenillaNuclear ProteinsProtein IsoformsProtein Kinase InhibitorsProtein Serine-Threonine KinasesRNA-Binding ProteinsSerine-Arginine Splicing FactorsSRPK1 protein, humanVascular Endothelial Growth Factor BVascular Endothelial Growth Factor Receptor-2VEGFB protein, humanWT1 Proteins

Identifiers

PMID22172722
PMCPMC3574979
OpenAlexW2027701384

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.