Evidence map›Paper›PMID 26025920›Full record

ArticleOncotarget2015

Melatonin antiproliferative effects require active mitochondrial function in embryonal carcinoma cells.

Rute Loureiro, Silvia Magalhães-Novais, Katia A Mesquita, Ines Baldeiras, Isabel S Sousa, Ludgero C Tavares, Ines A Barbosa, Paulo J Oliveira, Ignacio Vega-Naredo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Promising Antineoplastic Actions of Melatonin.Frontiers in pharmacology · 2018
    Review
  13. Melatonin, mitochondria, and the cancer cell.Cellular and molecular life sciences : CMLS · 2017
    Review
  14. Article
  15. Review
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 at 2 institutions in 2 countries.

Rute LoureiroCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Silvia Magalhães-NovaisCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Katia A MesquitaCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Ines BaldeirasCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Isabel S SousaCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Ludgero C TavaresCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Ines A BarbosaCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Paulo J OliveiraCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Ignacio Vega-NaredoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
University of Coimbra · PTUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although melatonin oncostatic and cytotoxic effects have been described in different types of cancer cells, the specific mechanisms leading to its antitumoral effects and their metabolic context specificity are still not completely understood. Here, we evaluated the effects of melatonin in P19 embryonal carcinoma stem cells (CSCs) and in their differentiated counterparts, cultured in either high glucose medium or in a galactose (glucose-free) medium which leads to glycolytic suppression and increased mitochondrial metabolism. We found that highly glycolytic P19 CSCs were less susceptible to melatonin antitumoral effects while cell populations relying on oxidative metabolism for ATP production were more affected. The observed antiproliferative action of melatonin was associated with an arrest at S-phase, decreased oxygen consumption, down-regulation of BCL-2 expression and an increase in oxidative stress culminating with caspase-3-independent cell death. Interestingly, the combined treatment of melatonin and dichloroacetate had a synergistic effect in cells grown in the galactose medium and resulted in an inhibitory effect in the highly resistant P19 CSCs. Melatonin appears to exert its antiproliferative activity in P19 carcinoma cells through a mitochondrially-mediated action which in turn allows the amplification of the effects of dichloroacetate, even in cells with a more glycolytic phenotype.

Indexed as

Antineoplastic AgentsBlotting, WesternCell Line, TumorCell ProliferationEmbryonal Carcinoma Stem CellsHumansMelatoninMembrane Potential, MitochondrialMitochondriaNeoplastic Stem CellsAntineoplastic AgentsMelatonincancer stem cellsdichloroacetatemelatoninmetabolismmitochondria

Identifiers

PMID26025920
PMCPMC4627293
OpenAlexW1951661930

What OpenQuestion holds

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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.