Evidence map›Paper›PMID 33609078›Full record

ArticleJournal of cellular and molecular medicine2021

The aberrant expression in epithelial cells of the mesenchymal isoform of FGFR2 controls the negative crosstalk between EMT and autophagy.

Danilo Ranieri, Monica Nanni, Luisa Guttieri, Maria Rosaria Torrisi, Francesca Belleudi

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Autophagy in chronic rhinosinusitis with or without nasal polyps.Frontiers in cell and developmental biology · 2024
    Review
  3. Article
  4. [Expression and significance of fibroblast growth factor receptor 2 in clear cell renal cell carcinoma].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022
    Article
  5. Article
  6. Article
  7. 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 3 institutions in 2 countries.

Danilo RanieriDepartment of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
Monica NanniDepartment of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
Luisa GuttieriDepartment of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
Maria Rosaria TorrisiDepartment of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.ORCID 0000-0003-2692-9312
Francesca BelleudiDepartment of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.ORCID 0000-0002-0773-0239
Sapienza University of Rome · ITCTO Andrea Alesini · ITUniversity Children's Hospital Zurich · CH

Funding

Progetti di Rilevante Interesse Nazionale PRIN 2017-Prot. 20174TB8KW
6 · The paper itself

Abstract

Signalling of the epithelial splicing variant of fibroblast growth factor receptor 2 (FGFR2b) triggers both differentiation and autophagy, while the aberrant expression of the mesenchymal FGFR2c isoform in epithelial cells induces impaired differentiation, inhibition of autophagy as well as the induction of the epithelial-mesenchymal transition (EMT). In light of the widely proposed negative loop linking autophagy and EMT in the early steps of carcinogenesis, here we investigated the possible involvement of FGFR2c aberrant expression and signalling in orchestrating this crosstalk in human keratinocytes. Biochemical, molecular, quantitative immunofluorescence analysis and in vitro invasion assays, coupled to the use of specific substrate inhibitors and transient or stable silencing approaches, showed that AKT/MTOR and PKCε are the two hub signalling pathways, downstream FGFR2c, intersecting with each other in the control of both the inhibition of autophagy and the induction of EMT and invasive behaviour. These results indicate that the expression of FGFR2c, possibly resulting from FGFR2 isoform switch, could represent a key upstream event responsible for the establishment of a negative interplay between autophagy and EMT, which contributes to the assessment of a pathological oncogenic profile in epithelial cells.

Indexed as

AutophagyCell DifferentiationEpithelial-Mesenchymal TransitionApoptosisCell ProliferationCells, CulturedEpithelial CellsHumansKeratinocytesMesodermProtein IsoformsReceptor, Fibroblast Growth Factor, Type 2Signal TransductionFGFR2 protein, humanProtein IsoformsReceptor, Fibroblast Growth Factor, Type 2autophagyEMTFGFR2cFGFRssignallingtumorigenesis

Identifiers

PMID33609078
PMCPMC8051744
OpenAlexW3129803643

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.