Evidence map›Paper›PMID 30054475›Full record

ArticleNature communications2018

Contact inhibition controls cell survival and proliferation via YAP/TAZ-autophagy axis.

Mariana Pavel, Maurizio Renna, So Jung Park, Fiona M Menzies, Thomas Ricketts, Jens Füllgrabe, Avraham Ashkenazi, Rebecca A Frake, Alejandro Carnicer Lombarte, Carla F Bento and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 1 pooled it
12.0field-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

179 citing papers in PubMed, 1 synthesis or guideline pooled it, 333 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Stress-dependent growth in breast cancer arises from a mechano-osmotic coupling and cell-sizing checkpoint.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. Review
  19. Article
  20. Drug design, development and therapy · 2026
    Review

119 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

12 authors at 5 institutions in 3 countries.

Mariana PavelDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Maurizio RennaDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
So Jung ParkDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Fiona M MenziesDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Thomas RickettsDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Jens FüllgrabeDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Avraham AshkenaziDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Rebecca A FrakeDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Alejandro Carnicer LombarteDepartment of Physiology Development and Neuroscience, University of Cambridge, CB2 3DY, Cambridge, UK.
Carla F BentoDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.ORCID http://orcid.org/0000-0001-8377-4543
Kristian FranzeDepartment of Physiology Development and Neuroscience, University of Cambridge, CB2 3DY, Cambridge, UK.
David C RubinszteinDepartment of Medical Genetics, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK. dcr1000@cam.ac.uk.
Wellcome Trust · GBUniversity of Cambridge · GBGrigore T. Popa University of Medicine and Pharmacy · ROUniversity of Naples Federico II · ITWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Medical Research Council UKDRI-2002Wellcome TrustWellcome Trust 095317/Z/11/Z
6 · The paper itself

Abstract

Contact inhibition enables noncancerous cells to cease proliferation and growth when they contact each other. This characteristic is lost when cells undergo malignant transformation, leading to uncontrolled proliferation and solid tumor formation. Here we report that autophagy is compromised in contact-inhibited cells in 2D or 3D-soft extracellular matrix cultures. In such cells, YAP/TAZ fail to co-transcriptionally regulate the expression of myosin-II genes, resulting in the loss of F-actin stress fibers, which impairs autophagosome formation. The decreased proliferation resulting from contact inhibition is partly autophagy-dependent, as is their increased sensitivity to hypoxia and glucose starvation. These findings define how mechanically repressed YAP/TAZ activity impacts autophagy to contribute to core phenotypes resulting from high cell confluence that are lost in various cancers.

Indexed as

Cell ProliferationActin CytoskeletonActinsAcyltransferasesAdaptor Proteins, Signal TransducingAnimalsApoptosisAutophagosomesAutophagyCapZ Actin Capping ProteinCell CountCell Line, TumorCell SurvivalContact InhibitionEpithelial CellsExtracellular MatrixActinsAcyltransferasesAdaptor Proteins, Signal TransducingCapZ Actin Capping ProteinCAPZB protein, humanGlucoseMyosin Type IIPhosphoproteinsTAFAZZIN protein, humanTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID30054475
PMCPMC6063886
OpenAlexW2884914303

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.