Evidence map›Paper›PMID 29068468›Full record

ArticleMolecular carcinogenesis2018

Expression of the FGFR2c mesenchymal splicing variant in human keratinocytes inhibits differentiation and promotes invasion.

Danilo Ranieri, Benedetta Rosato, Monica Nanni, Francesca Belleudi, Maria Rosaria Torrisi

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  6. Characterization of Alternative Splicing in High-Risk Wilms' Tumors.International journal of molecular sciences · 2024
    Article
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  13. Review
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  17. Alternative Splicing in Angiogenesis.International journal of molecular sciences · 2019
    Review
  18. Article
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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 2 institutions in 1 country.

Danilo RanieriLaboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Roma, Lazio, Italy.
Benedetta RosatoLaboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Roma, Lazio, Italy.
Monica NanniLaboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Roma, Lazio, Italy.
Francesca BelleudiLaboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Roma, Lazio, Italy.
Maria Rosaria TorrisiLaboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Roma, Lazio, Italy.ORCID 0000-0003-2692-9312
Istituto Pasteur · ITCTO Andrea Alesini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The altered isoform switching of the fibroblast growth factor receptor 2 (FGFR2) and aberrant expression of the mesenchymal FGFR2c isoform in epithelial cells is involved in cancer progression. We have recently described that the ectopic expression of FGFR2c in normal human keratinocytes induces epithelial-mesenchymal transition and leads to invasiveness and anchorage-independent growth. Here, we extended our analysis to the effects of this FGFR2c forced expression on human keratinocyte differentiation and stratification. Our findings demonstrated that, differently from cells overexpressing the epithelial splicing variant FGFR2b, keratinocytes ectopically expressing FGFR2c are not able to form a monolayer and display decreased expression of early differentiation markers. This impaired ability to enter the differentiation program is related to the up-modulation of the transcription factor ΔNp63. In addition, FGFR2c-expressing keratinocytes undergo defective stratification and invasion of the collagen matrix in 3D organotypic cultures, further suggesting their tumorigenic potential. Taken together, our results support the hypothesis that the receptor switching and the consequent appearance of the mesenchymal FGFR2c variant in the epithelial context would drive early steps of carcinogenesis, unbalancing the p63/FGFR interplay, and altering the paracrine response to the microenvironment.

Indexed as

Cell DifferentiationCell LineEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression RegulationHumansKeratinocytesNeoplasm InvasivenessProtein IsoformsReceptor, Fibroblast Growth Factor, Type 2RNA SplicingSignal TransductionFGFR2 protein, humanProtein IsoformsReceptor, Fibroblast Growth Factor, Type 2differentiationFGFR2human keratinocytesinvasion

Identifiers

PMID29068468
PMCPMC5813158
OpenAlexW2765779205

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.