Evidence map›Paper›PMID 34250755›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2021

mTOR Repression in Response to Amino Acid Starvation Promotes ECM Degradation Through MT1-MMP Endocytosis Arrest.

Cecilia Colombero, David Remy, Sandra Antoine-Bally, Anne-Sophie Macé, Pedro Monteiro, Nadia ElKhatib, Margot Fournier, Ahmed Dahmani, Elodie Montaudon, Guillaume Montagnac and 2 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Dietary Supplementation ofAnimals : an open access journal from MDPI · 2025
    Article
  8. NK cell activity in the tumor microenvironment.Frontiers in cell and developmental biology · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Cytoplasmic Tail of MT1-MMP: A Hub of MT1-MMP Regulation and Function.International journal of molecular sciences · 2023
    Review
  16. Review
  17. mTOR Signaling Components in Tumor Mechanobiology.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Review
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 3 institutions in 1 country.

Cecilia ColomberoInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.
David RemyInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.
Sandra Antoine-BallyInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.
Anne-Sophie MacéInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.
Pedro MonteiroInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.
Nadia ElKhatibGustave Roussy Institute, Université Paris-Saclay, INSERM U1279, Villejuif, 94805, France.
Margot FournierInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.
Ahmed DahmaniTranslational Research Department, Institut Curie, PSL Research University, Paris, 75005, France.
Elodie MontaudonTranslational Research Department, Institut Curie, PSL Research University, Paris, 75005, France.
Guillaume MontagnacGustave Roussy Institute, Université Paris-Saclay, INSERM U1279, Villejuif, 94805, France.
Elisabetta MarangoniTranslational Research Department, Institut Curie, PSL Research University, Paris, 75005, France.
Philippe ChavrierInstitut Curie, PSL Research University, CNRS UMR 144, Paris, 75005, France.ORCID 0000-0002-7351-733X
Centre National de la Recherche Scientifique · FRUniversité Paris Sciences et Lettres · FRInserm · FR

Funding

Fondation ARC pour la Recherche sur le Cancer ARCPGA12019120000973_1574
6 · The paper itself

Abstract

Under conditions of starvation, normal and tumor epithelial cells can rewire their metabolism toward the consumption of extracellular proteins, including extracellular matrix-derived components as nutrient sources. The mechanism of pericellular matrix degradation by starved cells has been largely overlooked. Here it is shown that matrix degradation by breast and pancreatic tumor cells and patient-derived xenograft explants increases by one order of magnitude upon amino acid and growth factor deprivation. In addition, it is found that collagenolysis requires the invadopodia components, TKS5, and the transmembrane metalloproteinase, MT1-MMP, which are key to the tumor invasion program. Increased collagenolysis is controlled by mTOR repression upon nutrient depletion or pharmacological inhibition by rapamycin. The results reveal that starvation hampers clathrin-mediated endocytosis, resulting in MT1-MMP accumulation in arrested clathrin-coated pits. The study uncovers a new mechanism whereby mTOR repression in starved cells leads to the repurposing of abundant plasma membrane clathrin-coated pits into robust ECM-degradative assemblies.

Indexed as

EndocytosisAmino AcidsAnimalsBreast NeoplasmsCell Line, TumorExtracellular MatrixFemaleHumansMatrix Metalloproteinase 14MiceTOR Serine-Threonine KinasesAmino AcidsMatrix Metalloproteinase 14MTOR protein, humanTOR Serine-Threonine Kinasesbreast cancerclathrin-mediated endocytosisextracellular matrixinvadopodiaMT1-MMPmTORstarvation

Identifiers

PMID34250755
PMCPMC8425857
OpenAlexW3182668743

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.