Evidence map›Paper›PMID 7803853›Full record

ArticleMolecular biology of the cell1994

Alternative splicing in fibroblast growth factor receptor 2 is associated with induced epithelial-mesenchymal transition in rat bladder carcinoma cells.

P Savagner, A M Vallés, J Jouanneau, K M Yamada, J P Thiery

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

56 citing papers in PubMed, 130 citations in OpenAlex.

  1. Alternative Splicing in Embryo Implantation.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2025
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Alternative Splicing in Angiogenesis.International journal of molecular sciences · 2019
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Connecting the dots: chromatin and alternative splicing in EMT.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016
    Review
  14. Role of EMT in Metastasis and Therapy Resistance.Journal of clinical medicine · 2016
    Review
  15. The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016
    Review
  16. A novel splice variant of XIAP-associated factor 1 (XAF1) is expressed in peripheral blood containing gastric cancer-derived circulating tumor cells.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2015
    Article
  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

5 authors at 1 institution in 2 countries.

P SavagnerLaboratoire de Physiopathologie du Développement, Centre National de la Recherche Scientifique-Ecole Normale Supérieure, Paris, France.
A M Vallés
J Jouanneau
K M Yamada
J P Thiery
École Normale Supérieure · BI

Funding

MULTIFUNCTIONAL GROWTH FACTORS IN TUMOR PROGRESSIONR01CA049417 · NCI · NATIONAL CENTER FOR SCIENTIFIC RESEARCH · PI THIERY, JEAN P · 1990 to 1995
–
NCI NIH HHS 2 R01 CA-49417-04
6 · The paper itself

Abstract

We described previously that acidic fibroblast growth factor (aFGF), but not basic fibroblast growth factor (bFGF), can induce the rat carcinoma cell line NBT-II to undergo a rapid and reversible transition from epithelial to mesenchymal phenotype (EMT). We now find that NBT-II EMT is stimulated by keratinocyte growth factor (KGF) in cells grown at low density. Accordingly, a high-affinity receptor showing 98% homology to mouse FGF receptor 2b/KGF receptor was cloned and sequenced from NBT-II cells. Northern analysis indicated that mRNA for FGF receptor 2b/KGF receptor was drastically down-regulated within 1 wk in aFGF-induced mesenchymal NBT-II cells. This decrease coincided with an up-regulation of FGF receptor 2c/Bek, a KGF-insensitive, alternatively spliced form of FGF receptor 2b/KGF receptor. Functional studies confirmed that KGF could not maintain EMT induction on mesenchymal NBT-II cells. FGF receptor 1 and FGF receptor 2c/Bek could also support EMT induction when transfected into NBT-II cells in response to aFGF or bFGF. Such transfected cells could bind bFGF as well as aFGF. Therefore, EMT can be induced through different FGF receptors, but EMT may also regulate FGF receptor expression itself.

Indexed as

Alternative SplicingAmino Acid SequenceAnimalsBase SequenceDNA PrimersEpitheliumGene Expression Regulation, NeoplasticHumansMesodermMiceMolecular Sequence DataPhenotypeRatsReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptor Protein-Tyrosine KinasesDNA PrimersFGFR1 protein, humanFgfr1 protein, mouseFgfr1 protein, ratFGFR2 protein, humanFgfr2 protein, mouseFgfr2 protein, ratkeratinocyte growth factor receptorReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptor Protein-Tyrosine KinasesReceptors, Fibroblast Growth FactorReceptors, Growth FactorRNA, Messenger

Identifiers

PMID7803853
PMCPMC301106
OpenAlexW2011151090

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.