Evidence map›Paper›PMID 24832466›Full record

ArticleCell death and differentiation2014

Mitochondrial metabolism directs stemness and differentiation in P19 embryonal carcinoma stem cells.

I Vega-Naredo, R Loureiro, K A Mesquita, I A Barbosa, L C Tavares, A F Branco, J R Erickson, J Holy, E L Perkins, R A Carvalho and 1 more

Abstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

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  11. The impact of mitochondria on cancer treatment resistance.Cellular oncology (Dordrecht, Netherlands) · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Targeting cancer stem cells from a metabolic perspective.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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.

I Vega-NaredoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.
R LoureiroCNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.
K A Mesquita1] CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal [2] Department of Life Sciences, University of Coimbra, 3004-517 Coimbra, Portugal.
I A BarbosaCNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.
L C Tavares1] CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal [2] Department of Life Sciences, University of Coimbra, 3004-517 Coimbra, Portugal.
A F BrancoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.
J R EricksonChicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.
J HolyDepartment of Biomedical Sciences, University of Minnesota-Duluth, Duluth, MN 55812, USA.
E L PerkinsDepartment of Biomedical Sciences, Mercer University School of Medicine, Savannah, GA 31404, USA.
R A Carvalho1] CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal [2] Department of Life Sciences, University of Coimbra, 3004-517 Coimbra, Portugal.
P J OliveiraCNC-Center for Neuroscience and Cell Biology, University of Coimbra, UC Biotech Building, Lot 8A, Biocant Park, 3060-197 Cantanhede, Portugal.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The relationship between mitochondrial metabolism and cell viability and differentiation in stem cells (SCs) remains poorly understood. In the present study, we compared mitochondrial physiology and metabolism between P19SCs before/after differentiation and present a unique fingerprint of the association between mitochondrial activity, cell differentiation and stemness. In comparison with their differentiated counterparts, pluripotency of P19SCs was correlated with a strong glycolytic profile and decreased mitochondrial biogenesis and complexity: round, low-polarized and inactive mitochondria with a closed permeability transition pore. This decreased mitochondrial capacity increased their resistance against dichloroacetate. Thus, stimulation of mitochondrial function by growing P19SCs in glutamine/pyruvate-containing medium reduced their glycolytic phenotype, induced loss of pluripotent potential, compromised differentiation and became P19SCs sensitive to dichloroacetate. Because of the central role of this type of SCs in teratocarcinoma development, our findings highlight the importance of mitochondrial metabolism in stemness, proliferation, differentiation and chemoresistance. In addition, the present work suggests the regulation of mitochondrial metabolism as a tool for inducing cell differentiation in stem line therapies.

Indexed as

Adenosine TriphosphateAnimalsCell DifferentiationCell ProliferationCell SurvivalDichloroacetic AcidDNA Copy Number VariationsEmbryonal Carcinoma Stem CellsEnergy MetabolismGlucoseMembrane Potential, MitochondrialMiceMitochondriaNeoplastic Stem CellsOxygen ConsumptionPluripotent Stem CellsAdenosine TriphosphateDichloroacetic AcidGlucose

Identifiers

PMID24832466
PMCPMC4158682

What OpenQuestion holds

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Registered trials

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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.