Evidence map›Paper›PMID 36325358›Full record

ArticleFrontiers in cell and developmental biology2022

Metabolic fingerprinting of chemotherapy-resistant prostate cancer stem cells. An untargeted metabolomic approach by liquid chromatography-mass spectrometry.

Alicia Bort, Belén G Sánchez, Carlos León, Leonor Nozal, José M Mora-Rodríguez, Florentina Castro, Antonio L Crego, Inés Díaz-Laviada

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. 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

8 authors.

Alicia BortYale University School of Medicine, Vascular Biology and Therapeutics Program, New Haven, CT, United states.
Belén G SánchezAlcala University, School of Medicine, Department of Systems Biology and Research Institute in Chemistry "Andrés M. Del Río" (IQAR), Madrid, Spain.
Carlos LeónCarlos III University, Department of Bioengineering and Aerospatial Engineering, Madrid, Spain.
Leonor NozalAlcala University and General Foundation of Alcalá University, Center of Applied Chemistry and Biotechnology, Madrid, Spain.
José M Mora-RodríguezAlcala University, School of Medicine, Department of Systems Biology and Research Institute in Chemistry "Andrés M. Del Río" (IQAR), Madrid, Spain.
Florentina CastroAlcala University and General Foundation of Alcalá University, Center of Applied Chemistry and Biotechnology, Madrid, Spain.
Antonio L CregoAlcala University, Department of Analytical Chemistry, Physical Chemistry and Chemical Engineering, Madrid, Spain.
Inés Díaz-LaviadaAlcala University, School of Medicine, Department of Systems Biology and Research Institute in Chemistry "Andrés M. Del Río" (IQAR), Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is one of the most important challenges in cancer therapy. The presence of cancer stem cells within the tumor may contribute to chemotherapy resistance since these cells express high levels of extrusion pumps and xenobiotic metabolizing enzymes that inactivate the therapeutic drug. Despite the recent advances in cancer cell metabolism adaptations, little is known about the metabolic adaptations of the cancer stem cells resistant to chemotherapy. In this study, we have undertaken an untargeted metabolomic analysis by liquid chromatography-high-resolution spectrometry combined with cytotoxicity assay, western blot, quantitative real-time polymerase chain reaction (qPCR), and fatty acid oxidation in a prostate cancer cell line resistant to the antiandrogen 2-hydroxiflutamide with features of cancer stem cells, compared to its parental androgen-sensitive cell line. Metabolic fingerprinting revealed 106 out of the 850 metabolites in ESI+ and 67 out of 446 in ESI- with significant differences between the sensitive and the resistant cell lines. Pathway analysis performed with the unequivocally identified metabolites, revealed changes in pathways involved in energy metabolism as well as posttranscriptional regulation. Validation by enzyme expression analysis indicated that the chemotherapy-resistant prostate cancer stem cells were metabolically dormant with decreased fatty acid oxidation, methionine metabolism and ADP-ribosylation. Our results shed light on the pathways underlying the entry of cancer cells into dormancy that might contribute to the mechanisms of drug resistance.

Indexed as

cancer chemoresistancecancer stem cellsfatty acid oxidationliquid chromatography-mass spectrometryprostate canceruntargeted metabolomic

Identifiers

PMID36325358
PMCPMC9618794

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.