Evidence map›Paper›PMID 37079050›Full record

ArticleJournal of cancer research and clinical oncology2023

The role of the Nrf2/GSH antioxidant system in cisplatin resistance in malignant rhabdoid tumours.

Patricia Hannon Barroeta, Maureen J O'Sullivan, Daniela M Zisterer

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

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  7. Genome-scale knockout simulation and clustering analysis of drug-resistant breast cancer cells reveal drug sensitization targets.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

3 authors at 2 institutions in 1 country.

Patricia Hannon BarroetaSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Pearse St, Dublin, D02 R590, Ireland. hannonbp@tcd.ie.
Maureen J O'SullivanThe National Children's Research Centre, Children's Health Ireland at Crumlin, Dublin, D12 N512, Ireland.
Daniela M ZistererSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Pearse St, Dublin, D02 R590, Ireland.
Trinity College Dublin · IENational Children’s Research Centre · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMalignant rhabdoid tumour (MRT) is a rare and aggressive childhood malignancy that occurs in the kidneys or central nervous system and is associated with very poor prognosis. Chemoresistance is a major issue in the treatment of this malignancy leading to an urgent need for a greater understanding of its underlying mechanisms in MRT and novel treatment strategies for MRT patients. The balance between oxidative stress mediated by reactive oxygen species (ROS) and the antioxidant system has become a subject of interest in cancer therapy research. Studies have implicated key players of the antioxidant system in chemotherapeutic including the well-known antioxidant glutathione (GSH) and the transcription factor nuclear erythroid-related factor-2 (Nrf2).  

methodsThis study evaluated the role of these components in the response of MRT cells to treatment with the commonly used chemotherapeutic agent, cisplatin.

resultsThis study characterised the basal levels of GSH, ROS and Nrf2 in a panel of MRT cell lines and found a correlation between the expression profile of the antioxidant defence system and cisplatin sensitivity. Results showed that treatment with ROS scavenger N-acetylcysteine (NAC) protected cells from cisplatin-induced ROS and apoptosis. Interestingly, depleting GSH levels with the inhibitor buthionine sulphoximine (BSO) enhanced cisplatin-induced ROS and sensitised cells to cisplatin. Lastly, targeting Nrf2 with the small molecule inhibitor ML385 or by siRNA diminished GSH levels, enhanced ROS and sensitised resistant MRT cells to cisplatin.

conclusionsThese results suggest that targeting the Nrf2/GSH antioxidant system may present a novel therapeutic strategy to combat chemoresistance in rhabdoid tumours.

Indexed as

CisplatinRhabdoid TumorAntioxidantsApoptosisButhionine SulfoximineCell Line, TumorChildGlutathioneHumansNF-E2-Related Factor 2Reactive Oxygen SpeciesAntioxidantsButhionine SulfoximineCisplatinGlutathioneNF-E2-Related Factor 2Reactive Oxygen SpeciesApoptosisChemoresistanceGlutathioneMalignant rhabdoid tumourNuclear erythroid-related factor-2Reactive oxygen species

Identifiers

PMID37079050
PMCPMC10374708
OpenAlexW4366462748

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.