Evidence map›Paper›PMID 26355343›Full record

ArticleCell death & disease2015

Autophagy regulates hepatocyte identity and epithelial-to-mesenchymal and mesenchymal-to-epithelial transitions promoting Snail degradation.

G Grassi, G Di Caprio, L Santangelo, G M Fimia, A M Cozzolino, M Komatsu, G Ippolito, M Tripodi, T Alonzi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
8.3field-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

82 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
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  3. Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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22 more citing papers are in PubMed but not listed here.

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

9 authors at 6 institutions in 2 countries.

G GrassiNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
G Di CaprioNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
L SantangeloDepartment of Cellular Biotechnologies and Hematology, Pasteur Institute-Cenci Bolognetti Foundation, Sapienza University of Rome, Rome, Italy.
G M FimiaNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
A M CozzolinoNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
M KomatsuDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata, 951-8510, Japan.
G IppolitoNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
M TripodiNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
T AlonziNational Institute for Infectious Diseases L. Spallanzani IRCCS, Rome, Italy.
Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITIstituto Pasteur · ITNiigata University · JPSapienza University of Rome · ITUniversity of Salento · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) and the reverse process mesenchymal-to-epithelial transition (MET) are events involved in development, wound healing and stem cell behaviour and contribute pathologically to cancer progression. The identification of the molecular mechanisms underlying these phenotypic conversions in hepatocytes are fundamental to design specific therapeutic strategies aimed at optimising liver repair. The role of autophagy in EMT/MET processes of hepatocytes was investigated in liver-specific autophagy-deficient mice (Alb-Cre;ATG7(fl/fl)) and using the nontumorigenic immortalised hepatocytes cell line MMH. Autophagy deficiency in vivo reduces epithelial markers' expression and increases the levels of mesenchymal markers. These alterations are associated with an increased protein level of the EMT master regulator Snail, without transcriptional induction. Interestingly, we found that autophagy degrades Snail in a p62/SQSTM1 (Sequestosome-1)-dependent manner. Moreover, accordingly to a pro-epithelial function, we observed that autophagy stimulation strongly affects EMT progression, whereas it is necessary for MET. Finally, we found that the EMT induced by TGFβ affects the autophagy flux, indicating that these processes regulate each other. Overall, we found that autophagy regulates the phenotype plasticity of hepatocytes promoting their epithelial identity through the inhibition of the mesenchymal programme.

Indexed as

AnimalsAutophagyCell Line, TumorEpithelial-Mesenchymal TransitionMiceTranscription FactorsTranscription Factors

Identifiers

PMID26355343
PMCPMC4650445
OpenAlexW1784434253

What OpenQuestion 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 OpenQuestion graph.