Evidence map›Paper›PMID 28303926›Full record

ArticleScientific reports2017

Identification of the metabolic alterations associated with the multidrug resistant phenotype in cancer and their intercellular transfer mediated by extracellular vesicles.

Vanessa Lopes-Rodrigues, Alessio Di Luca, Justyna Mleczko, Paula Meleady, Michael Henry, Milica Pesic, Diana Cabrera, Sebastiaan van Liempd, Raquel T Lima, Robert O'Connor and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed.

  1. Article
  2. Article
  3. Paclitaxel resistance-associated metabolic events in ovarian cancer cells.Metabolomics : Official journal of the Metabolomic Society · 2025
    Article
  4. Article
  5. Review
  6. Discovery of Potent IsoquinolinequinoneJournal of medicinal chemistry · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

12 authors.

Vanessa Lopes-Rodriguesi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal.
Alessio Di LucaNICB - National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland.
Justyna MleczkoExosomes Laboratory &Metabolomics platform, CIC bioGUNE, CIBERehd, Derio, Spain.
Paula MeleadyNICB - National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland.
Michael HenryNICB - National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland.
Milica PesicInstitute for Biological Research "Sinisa Stankovic", University of Belgrade, Despota Stefana 142, 11060 Belgrade, Serbia.
Diana CabreraExosomes Laboratory &Metabolomics platform, CIC bioGUNE, CIBERehd, Derio, Spain.
Sebastiaan van LiempdExosomes Laboratory &Metabolomics platform, CIC bioGUNE, CIBERehd, Derio, Spain.
Raquel T Limai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal.
Robert O'ConnorNICB - National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland.
Juan M Falcon-PerezExosomes Laboratory &Metabolomics platform, CIC bioGUNE, CIBERehd, Derio, Spain.
M Helena Vasconcelosi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) is a serious obstacle to efficient cancer treatment. Overexpression of P-glycoprotein (P-gp) plays a significant role in MDR. Recent studies proved that targeting cellular metabolism could sensitize MDR cells. In addition, metabolic alterations could affect the extracellular vesicles (EVs) cargo and release. This study aimed to: i) identify metabolic alterations in P-gp overexpressing cells that could be involved in the development of MDR and, ii) identify a potential role for the EVs in the acquisition of the MDR. Two different pairs of MDR and their drug-sensitive counterpart cancer cell lines were used. Our results showed that MDR (P-gp overexpressing) cells have a different metabolic profile from their drug-sensitive counterparts, demonstrating decreases in the pentose phosphate pathway and oxidative phosphorylation rate; increases in glutathione metabolism and glycolysis; and alterations in the methionine/S-adenosylmethionine pathway. Remarkably, EVs from MDR cells were capable of stimulating a metabolic switch in the drug-sensitive cancer cells, towards a MDR phenotype. In conclusion, obtained results contribute to the growing knowledge about metabolic alterations in MDR cells and the role of EVs in the intercellular transfer of MDR. The specific metabolic alterations identified in this study may be further developed as targets for overcoming MDR.

Indexed as

Antineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1Drug Resistance, MultipleDrug Resistance, NeoplasmExtracellular VesiclesGene Expression Regulation, NeoplasticHumansK562 CellsMethionineNeoplasmsS-AdenosylmethionineAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily B, Member 1MethionineS-Adenosylmethionine

Identifiers

PMID28303926
PMCPMC5356019

What OpenQuestion holds

Textmetadata
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.