Evidence map›Paper›PMID 27545895›Full record

ArticleCell reports2016

PML at Mitochondria-Associated Membranes Is Critical for the Repression of Autophagy and Cancer Development.

Sonia Missiroli, Massimo Bonora, Simone Patergnani, Federica Poletti, Mariasole Perrone, Roberta Gafà, Eros Magri, Andrea Raimondi, Giovanni Lanza, Carlo Tacchetti and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
10.7field-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

90 citing papers in PubMed, 153 citations in OpenAlex.

  1. Review
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  3. A CHKA-PML autophagy checkpoint enables tumors to evade glutamine starvation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  5. Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.Apoptosis : an international journal on programmed cell death · 2026
    Review
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30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 4 countries.

Sonia MissiroliDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy.
Massimo BonoraDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy.
Simone PatergnaniDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy.
Federica PolettiDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy.
Mariasole PerroneDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy.
Roberta GafàDepartment of Morphology, Surgery and Experimental Medicine, Section of Anatomic Pathology and Molecular Diagnostics, University of Ferrara, Ferrara 44121, Italy.
Eros MagriDepartment of Morphology, Surgery and Experimental Medicine, Section of Anatomic Pathology and Molecular Diagnostics, University of Ferrara, Ferrara 44121, Italy.
Andrea RaimondiExperimental Imaging Center, San Raffaele Scientific Institute, Milan 20132, Italy.
Giovanni LanzaDepartment of Morphology, Surgery and Experimental Medicine, Section of Anatomic Pathology and Molecular Diagnostics, University of Ferrara, Ferrara 44121, Italy.
Carlo TacchettiExperimental Imaging Center, San Raffaele Scientific Institute, Milan 20132, Italy; Department of Experimental Medicine, University of Genoa, Genoa 16132, Italy.
Guido KroemerEquipe 11 Labellisée par la Ligue contre le Cancer, Centre de Recherche des Cordeliers, Paris 75006, France; Cell Biology and Metabolomics platforms, Gustave Roussy Comprehensive Cancer Center, Villejuif 94800, France; INSERM, U1138, Paris 75006, France; Université Paris Descartes, Sorbonne Paris Cité, Paris 75006, France; Université Pierre et Marie Curie, Paris VI, Paris 75006, France; Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris 75015, France; Karolinska Institute and Department of Women's and Children's Health, Karolinska University Hospital Q2:07, 17176 Stockholm, Sweden.
Pier Paolo PandolfiCancer Genetics Program, Beth Israel Deaconess Cancer Center, Harvard Medical School, Boston, MA 02215, USA; Departments of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Paolo PintonDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy.
Carlotta GiorgiDepartment of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology and LTTA Center, University of Ferrara, Ferrara 44121, Italy. Electronic address: grgclt@unife.it.
University of Ferrara · ITSan Raffaele University of Rome · ITBeth Israel Deaconess Medical Center · USInstitut Gustave Roussy · FR

Funding

Telethon GGP15219
6 · The paper itself

Abstract

The precise molecular mechanisms that coordinate apoptosis and autophagy in cancer remain to be determined. Here, we provide evidence that the tumor suppressor promyelocytic leukemia protein (PML) controls autophagosome formation at mitochondria-associated membranes (MAMs) and, thus, autophagy induction. Our in vitro and in vivo results demonstrate how PML functions as a repressor of autophagy. PML loss promotes tumor development, providing a growth advantage to tumor cells that use autophagy as a cell survival strategy during stress conditions. These findings demonstrate that autophagy inhibition could be paired with a chemotherapeutic agent to develop anticancer strategies for tumors that present PML downregulation.

Indexed as

Gene Expression Regulation, NeoplasticAdenineAnimalsAntineoplastic AgentsArsenicalsArsenic TrioxideAutophagyCalciumCell Line, TumorDisease ProgressionFibroblastsHumansLeukemia, Promyelocytic, AcuteMembrane Potential, MitochondrialMiceMice, Knockout3-methyladenineAdenineAntineoplastic AgentsArsenicalsArsenic TrioxideCalciumOncogene Proteins, FusionOxidesPML protein, humanPml protein, mousePromyelocytic Leukemia Proteinpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinTumor Suppressor Protein p53

Identifiers

PMID27545895
PMCPMC5011426
OpenAlexW2514431030

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.