Evidence map›Paper›PMID 31416916›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Cell phenotypic plasticity requires autophagic flux driven by YAP/TAZ mechanotransduction.

Antonio Totaro, Qiuyu Zhuang, Tito Panciera, Giusy Battilana, Luca Azzolin, Giulia Brumana, Alessandro Gandin, Giovanna Brusatin, Michelangelo Cordenonsi, Stefano Piccolo

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 157 citations in OpenAlex.

  1. Review
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  5. Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  15. Hapalindole Q suppresses autophagosome-lysosome fusion by promoting YAP1 degradation via chaperon-mediated autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  16. Article
  17. Review
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21 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

10 authors at 1 institution in 1 country.

Antonio TotaroDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Qiuyu ZhuangDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Tito PancieraDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Giusy BattilanaDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Luca AzzolinDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Giulia BrumanaDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Alessandro GandinDepartment of Industrial Engineering, University of Padua, 35131 Padua, Italy.
Giovanna BrusatinDepartment of Industrial Engineering, University of Padua, 35131 Padua, Italy.
Michelangelo CordenonsiDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy.
Stefano PiccoloDepartment of Molecular Medicine, University of Padua School of Medicine, 35131 Padua, Italy; piccolo@bio.unipd.it.
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, besides ensuring energy metabolism and organelle renewal, is crucial for the biology of adult normal and cancer stem cells. However, it remains incompletely understood how autophagy connects to stemness factors and the nature of the microenvironmental signals that pattern autophagy in different cell types. Here we advance in these directions by reporting that YAP/TAZ transcriptionally control autophagy, being critical for autophagosomal degradation into autolysosomes. YAP/TAZ are downstream effectors of cellular mechanotransduction and indeed we found that cell mechanics, dictated by the physical property of the ECM and cytoskeletal tension, profoundly impact on autophagic flux in a YAP/TAZ-mediated manner. Functionally, by using pancreatic and mammary organoid cultures, we found that YAP/TAZ-regulated autophagy is essential in normal cells for YAP/TAZ-mediated dedifferentiation and acquisition of self-renewing properties. In tumor cells, the YAP/TAZ-autophagy connection is key to sustain transformed traits and for acquisition of a cancer stem cell state by otherwise more benign cells. Mechanistically, YAP/TAZ promote autophagic flux by directly promoting the expression of Armus, a RAB7-GAP required for autophagosome turnover and whose add-back rescues autophagy in YAP/TAZ-depleted cells. These findings expand the influence of YAP/TAZ mechanotransduction to the control of autophagy and, vice versa, the role of autophagy in YAP/TAZ biology, and suggest a mechanism to coordinate transcriptional rewiring with cytoplasmic restructuring during cell reprogramming.

Indexed as

AutophagyCell PlasticityMechanotransduction, CellularAcyltransferasesAdaptation, PhysiologicalAnimalsAutophagosomesCell Cycle ProteinsHumansLysosomesProtein BindingProteolysisTranscription FactorsAcyltransferasesCell Cycle ProteinsTAFAZZIN protein, humanTranscription FactorsYY1AP1 protein, humanautophagycell plasticitymechanotransductionYAP/TAZ

Identifiers

PMID31416916
PMCPMC6731754
OpenAlexW2969022049

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.