Evidence map›Paper›PMID 29374163›Full record

ArticleNature communications2018

Mitochondrial levels determine variability in cell death by modulating apoptotic gene expression.

Silvia Márquez-Jurado, Juan Díaz-Colunga, Ricardo Pires das Neves, Antonio Martinez-Lorente, Fernando Almazán, Raúl Guantes, Francisco J Iborra

Abstract 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 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

81 citing papers in PubMed, 1 synthesis or guideline pooled it.

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21 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

7 authors.

Silvia Márquez-JuradoDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, 28049, Madrid, Spain.ORCID http://orcid.org/0000-0003-4592-9756
Juan Díaz-ColungaDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, 28049, Madrid, Spain.
Ricardo Pires das NevesUC-Biotech, Center for Neuroscience and Cell Biology (CNC), Biocant, Center of Innovation in Biotechnology, 3060-197, Cantanhede, Portugal.
Antonio Martinez-LorenteDepartment of Pathology of Torrevieja and Vinalopó Hospitals, 031186, Alicante, Spain.
Fernando AlmazánDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, 28049, Madrid, Spain.
Raúl GuantesDepartment of Condensed Matter Physics, Materials Science Institute "Nicolás Cabrera" and Institute of Condensed Matter Physics (IFIMAC), Universidad Autónoma de Madrid, Campus de Cantoblanco, 28049, Madrid, Spain. raul.guantes@uam.es.
Francisco J IborraDepartment of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, 28049, Madrid, Spain. fjiborra@cnb.csic.es.ORCID http://orcid.org/0000-0002-0692-3696

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fractional killing is the main cause of tumour resistance to chemotherapy. This phenomenon is observed even in genetically identical cancer cells in homogeneous microenvironments. To understand this variable resistance, here we investigate the individual responses to TRAIL in a clonal population of HeLa cells using live-cell microscopy and computational modelling. We show that the cellular mitochondrial content determines the apoptotic fate and modulates the time to death, cells with higher mitochondrial content are more prone to die. We find that all apoptotic protein levels are modulated by the mitochondrial content. Modelling the apoptotic network, we demonstrate that these correlations, and especially the differential control of anti- and pro-apoptotic protein pairs, confer mitochondria a powerful discriminatory capacity of apoptotic fate. We find a similar correlation between the mitochondria and apoptotic proteins in colon cancer biopsies. Our results reveal a different role of mitochondria in apoptosis as the global regulator of apoptotic protein expression.

Indexed as

AlgorithmsApoptosisApoptosis Regulatory ProteinsCell DeathGene ExpressionHeLa CellsHumansMitochondriaModels, GeneticReactive Oxygen SpeciesSignal TransductionTNF-Related Apoptosis-Inducing LigandApoptosis Regulatory ProteinsReactive Oxygen SpeciesTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID29374163
PMCPMC5785974

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.