Evidence map›Paper›PMID 34825138›Full record

ArticleiScience2021

Metabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdown.

Adam Krysztofiak, Klaudia Szymonowicz, Julian Hlouschek, Kexu Xiang, Christoph Waterkamp, Safa Larafa, Isabell Goetting, Silvia Vega-Rubin-de-Celis, Carsten Theiss, Veronika Matschke and 3 more

Abstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

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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

13 authors.

Adam KrysztofiakInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Klaudia SzymonowiczInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Julian HlouschekInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Kexu XiangInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Christoph WaterkampBioinformatics and Computational Biophysics, University of Duisburg-Essen, 45117 Essen, Germany.
Safa LarafaInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Isabell GoettingInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Silvia Vega-Rubin-de-CelisInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Carsten TheissDepartment of Cytology, Institute of Anatomy, Medical Faculty, Ruhr University Bochum, 44801 Bochum, Germany.
Veronika MatschkeDepartment of Cytology, Institute of Anatomy, Medical Faculty, Ruhr University Bochum, 44801 Bochum, Germany.
Daniel HoffmannBioinformatics and Computational Biophysics, University of Duisburg-Essen, 45117 Essen, Germany.
Verena JendrossekInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Johann MatschkeInstitute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer bioenergetics fuel processes necessary to maintain viability and growth under stress conditions. We hypothesized that cancer metabolism supports the repair of radiation-induced DNA double-stranded breaks (DSBs). We combined the systematic collection of metabolic and radiobiological data from a panel of irradiated cancer cell lines with mathematical modeling and identified a common metabolic response with impact on the DSB repair kinetics, including a mitochondrial shutdown followed by compensatory glycolysis and resumption of mitochondrial function. Combining ionizing radiation (IR) with inhibitors of the compensatory glycolysis or mitochondrial respiratory chain slowed mitochondrial recovery and DNA repair kinetics, offering an opportunity for therapeutic intervention. Mathematical modeling allowed us to generate new hypotheses on general and individual mechanisms of the radiation response with relevance to DNA repair and on metabolic vulnerabilities induced by cancer radiotherapy. These discoveries will guide future mechanistic studies for the discovery of metabolic targets for overcoming intrinsic or therapy-induced radioresistance.

Indexed as

CancerCancer systems biologyMathematical biosciences

Identifiers

PMID34825138
PMCPMC8603201

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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.