Evidence map›Paper›PMID 25438055›Full record

ArticleNature cell biology2015

AMBRA1 links autophagy to cell proliferation and tumorigenesis by promoting c-Myc dephosphorylation and degradation.

Valentina Cianfanelli, Claudia Fuoco, Mar Lorente, Maria Salazar, Fabio Quondamatteo, Pier Federico Gherardini, Daniela De Zio, Francesca Nazio, Manuela Antonioli, Melania D'Orazio and 12 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 153 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 2 pooled it
14.6field-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

153 citing papers in PubMed, 2 syntheses or guidelines pooled it, 259 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Autophagy modulation in cancer.Nature reviews. Drug discovery · 2026
    Review
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93 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 9 institutions in 5 countries.

Valentina Cianfanelli1] Unit of Cell Stress and Survival, Danish Cancer Society Research Center, 2100 Copenhagen, Denmark [2] Laboratory of Molecular Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy.
Claudia FuocoDepartment of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy.
Mar Lorente1] Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain [2] Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain.
Maria Salazar1] Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain [2] Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain.
Fabio QuondamatteoSkin and Extracellular Matrix Research Group, Anatomy NUI Galway, Ireland.
Pier Federico GherardiniDepartment of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy.
Daniela De ZioUnit of Cell Stress and Survival, Danish Cancer Society Research Center, 2100 Copenhagen, Denmark.
Francesca NazioLaboratory of Molecular Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy.
Manuela Antonioli1] Department of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy [2] National Institute for Infectious Diseases IRCCS 'L. Spallanzani', 00149 Rome, Italy.
Melania D'OrazioDepartment of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy.
Tatjana SkoboDepartment of Biology, University of Padua, 35131 Padua, Italy.
Matteo BordiLaboratory of Molecular Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy.
Mikkel RohdeUnit of Cell Death and Metabolism, Danish Cancer Society Research Center, 2100 Copenhagen, Denmark.
Luisa Dalla ValleDepartment of Biology, University of Padua, 35131 Padua, Italy.
Manuela Helmer-CitterichDepartment of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy.
Christine Gretzmeier1] Department of Dermatology, University Freiburg Medical Center, 79104 Freiburg, Germany [2] ZBSA Center for Biological Systems Analysis, University of Freiburg, 79104 Freiburg, Germany.
Joern Dengjel1] Department of Dermatology, University Freiburg Medical Center, 79104 Freiburg, Germany [2] ZBSA Center for Biological Systems Analysis, University of Freiburg, 79104 Freiburg, Germany.
Gian Maria Fimia1] National Institute for Infectious Diseases IRCCS 'L. Spallanzani', 00149 Rome, Italy [2] Department of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, Lecce 73100, Italy.
Mauro Piacentini1] Department of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy [2] National Institute for Infectious Diseases IRCCS 'L. Spallanzani', 00149 Rome, Italy.
Sabrina Di BartolomeoDepartment of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy.
Guillermo Velasco1] Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain [2] Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain.
Francesco Cecconi1] Unit of Cell Stress and Survival, Danish Cancer Society Research Center, 2100 Copenhagen, Denmark [2] Laboratory of Molecular Neuroembryology, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy [3] Department of Biology, University of Rome 'Tor Vergata', 00133 Rome, Italy.
University of Rome Tor Vergata · ITDanish Cancer Society · DKIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversidad Complutense de Madrid · ESUniversity Medical Center Freiburg · DEUniversity of Padua · ITFondazione Santa Lucia · ITInstituto de Investigación Sanitaria del Hospital Clínico San Carlos · ESOllscoil na Gaillimhe – University of Galway · IE

Funding

Telethon GGP10225
6 · The paper itself

Abstract

Inhibition of a main regulator of cell metabolism, the protein kinase mTOR, induces autophagy and inhibits cell proliferation. However, the molecular pathways involved in the cross-talk between these two mTOR-dependent cell processes are largely unknown. Here we show that the scaffold protein AMBRA1, a member of the autophagy signalling network and a downstream target of mTOR, regulates cell proliferation by facilitating the dephosphorylation and degradation of the proto-oncogene c-Myc. We found that AMBRA1 favours the interaction between c-Myc and its phosphatase PP2A and that, when mTOR is inhibited, it enhances PP2A activity on this specific target, thereby reducing the cell division rate. As expected, such a de-regulation of c-Myc correlates with increased tumorigenesis in AMBRA1-defective systems, thus supporting a role for AMBRA1 as a haploinsufficient tumour suppressor gene.

Indexed as

HaploinsufficiencyAdaptor Proteins, Signal TransducingAnimalsAutophagyCell DivisionCell Line, TumorCell Transformation, NeoplasticFemaleGenes, Tumor SuppressorHEK293 CellsHeLa CellsHumansMaleMiceMice, Inbred C57BLMice, TransgenicAdaptor Proteins, Signal TransducingAMBRA1 protein, humanAmbra1 protein, mouseMAS1 protein, humanMTOR protein, humanMYC protein, humanProtein Phosphatase 2Proto-Oncogene MasProto-Oncogene Proteins c-mycRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID25438055
PMCPMC4976803
OpenAlexW2009874228

What OpenQuestion holds

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Registered trials

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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.