Evidence map›Paper›PMID 28112156›Full record

ArticleNature communications2017

mTORC1 inhibition in cancer cells protects from glutaminolysis-mediated apoptosis during nutrient limitation.

Victor H Villar, Tra Ly Nguyen, Vanessa Delcroix, Silvia Terés, Marion Bouchecareilh, Bénédicte Salin, Clément Bodineau, Pierre Vacher, Muriel Priault, Pierre Soubeyran and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

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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

11 authors at 5 institutions in 1 country.

Victor H VillarInstitut Européen de Chimie et Biologie, INSERM U1218, Université de Bordeaux, 2 Rue Robert Escarpit, Pessac 33607, France.
Tra Ly NguyenInstitut Européen de Chimie et Biologie, INSERM U1218, Université de Bordeaux, 2 Rue Robert Escarpit, Pessac 33607, France.
Vanessa DelcroixInstitut Bergonié, INSERM U1218, 229 Cours de l'Argonne, Bordeaux 33076, France.
Silvia TerésInstitut Européen de Chimie et Biologie, INSERM U1218, Université de Bordeaux, 2 Rue Robert Escarpit, Pessac 33607, France.
Marion BouchecareilhInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 Rue Camille Saint-Saëns, Bordeaux 33077, France.
Bénédicte SalinInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 Rue Camille Saint-Saëns, Bordeaux 33077, France.
Clément BodineauInstitut Européen de Chimie et Biologie, INSERM U1218, Université de Bordeaux, 2 Rue Robert Escarpit, Pessac 33607, France.
Pierre VacherInstitut Bergonié, INSERM U1218, 229 Cours de l'Argonne, Bordeaux 33076, France.
Muriel PriaultInstitut de Biochimie et Génétique Cellulaires, CNRS UMR 5095, Université de Bordeaux, 1 Rue Camille Saint-Saëns, Bordeaux 33077, France.
Pierre SoubeyranInstitut Bergonié, INSERM U1218, 229 Cours de l'Argonne, Bordeaux 33076, France.
Raúl V DuránInstitut Européen de Chimie et Biologie, INSERM U1218, Université de Bordeaux, 2 Rue Robert Escarpit, Pessac 33607, France.
Centre National de la Recherche Scientifique · FRInserm · FRInstitut Bergonié · FRUniversité de Bordeaux · FRInstitut Européen de Chimie et Biologie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A master coordinator of cell growth, mTORC1 is activated by different metabolic inputs, particularly the metabolism of glutamine (glutaminolysis), to control a vast range of cellular processes, including autophagy. As a well-recognized tumour promoter, inhibitors of mTORC1 such as rapamycin have been approved as anti-cancer agents, but their overall outcome in patients is rather poor. Here we show that mTORC1 also presents tumour suppressor features in conditions of nutrient restrictions. Thus, the activation of mTORC1 by glutaminolysis during nutritional imbalance inhibits autophagy and induces apoptosis in cancer cells. Importantly, rapamycin treatment reactivates autophagy and prevents the mTORC1-mediated apoptosis. We also observe that the ability of mTORC1 to activate apoptosis is mediated by the adaptor protein p62. Thus, the mTORC1-mediated upregulation of p62 during nutrient imbalance induces the binding of p62 to caspase 8 and the subsequent activation of the caspase pathway. Our data highlight the role of autophagy as a survival mechanism upon rapamycin treatment.

Indexed as

AntibodiesApoptosisAutophagyCell Line, TumorCulture MediaGene Expression RegulationGlutamineHumansMechanistic Target of Rapamycin Complex 1PlasmidsRNA, MessengerAntibodiesCulture MediaGlutamineMechanistic Target of Rapamycin Complex 1RNA, Messenger

Identifiers

PMID28112156
PMCPMC5264013
OpenAlexW2580339440

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.