Evidence map›Paper›PMID 40185729›Full record

ArticleCell death & disease2025

Mitochondrial, metabolic and bioenergetic adaptations drive plasticity of colorectal cancer cells and shape their chemosensitivity.

Nikita Markov, Sirina Sabirova, Gulnaz Sharapova, Marina Gomzikova, Anna Brichkina, Nick A Barlev, Marcel Egger, Albert Rizvanov, Hans-Uwe Simon

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Mapping malignant T-cell states and immune circuits in Sézary syndrome by single-cell analysis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
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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

9 authors.

Nikita MarkovInstitute of Pharmacology, University of Bern, Bern, Switzerland.ORCID http://orcid.org/0000-0003-1121-973X
Sirina SabirovaLaboratory of Molecular Immunology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Gulnaz SharapovaLaboratory of Molecular Immunology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Marina GomzikovaLaboratory of Molecular Immunology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Anna BrichkinaInstitute of Systems Immunology, Center for Tumor Biology and Immunology, Philipps University of Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0001-8707-9900
Nick A BarlevLaboratory of Molecular Immunology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Marcel EggerDepartment of Physiology, University of Bern, Bern, Switzerland.ORCID http://orcid.org/0000-0002-4247-3629
Albert RizvanovOpenLab Gene and Cell Technology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.ORCID http://orcid.org/0000-0002-9427-5739
Hans-Uwe SimonInstitute of Pharmacology, University of Bern, Bern, Switzerland. hans-uwe.simon@unibe.ch.ORCID http://orcid.org/0000-0002-9404-7736

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 310030_184816
6 · The paper itself

Abstract

The extent of mitochondrial heterogeneity and the presence of mitochondrial archetypes in cancer remain unknown. Mitochondria play a central role in the metabolic reprogramming that occurs in cancer cells. This process adjusts the activity of metabolic pathways to support growth, proliferation, and survival of cancer cells. Using a panel of colorectal cancer (CRC) cell lines, we revealed extensive differences in their mitochondrial composition, suggesting functional specialisation of these organelles. We differentiated bioenergetic and mitochondrial phenotypes, which point to different strategies used by CRC cells to maintain their sustainability. Moreover, the efficacy of various treatments targeting metabolic pathways was dependent on the respiration and glycolysis levels of cancer cells. Furthermore, we identified metabolites associated with both bioenergetic profiles and cell responses to treatments. The levels of these molecules can be used to predict the therapeutic efficacy of anti-cancer drugs and identify metabolic vulnerabilities of CRC. Our study indicates that the efficacy of CRC therapies is closely linked to mitochondrial status and cellular bioenergetics.

Indexed as

Adaptation, PhysiologicalCell PlasticityColorectal NeoplasmsEnergy MetabolismMitochondriaAntineoplastic AgentsCell Line, TumorCell ProliferationGlycolysisHumansAntineoplastic Agents

Identifiers

PMID40185729
PMCPMC11971274

What OpenQuestion holds

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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.