Evidence map›Paper›PMID 40387816›Full record

ArticleOncotarget2025

PRDX1 protects ATM from arsenite-induced proteotoxicity and maintains its stability during DNA damage signaling.

Reem Ali, Mashael Algethami, Amera Sheha, Shatha Alqahtani, Ahmad Altayyar, Ayat Lashen, Emad Rakha, Abdallah Alhaj Sulaiman, Srinivasan Madhusudan, Dindial Ramotar

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In one paragraph

Article in Oncotarget, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Reem AliCollege of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar.
Mashael AlgethamiNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Amera ShehaNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Shatha AlqahtaniNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Ahmad AltayyarNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Ayat LashenNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Emad RakhaNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Abdallah Alhaj SulaimanCollege of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar.
Srinivasan MadhusudanNaaz Coker Ovarian Cancer Research Centre, Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Dindial RamotarCollege of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Redox regulation and DNA repair coordination are essential for genomic stability. Peroxiredoxin 1 (PRDX1) is a thiol-dependent peroxidase and a chaperone that protects proteins from excessive oxidation. ATM kinase (Ataxia-Telangiectasia Mutated) and the MRN (MRE11-RAD50-NBS1) complex are DNA damage signaling and repair proteins. We previously showed that cells lacking PRDX1 are sensitive to arsenite, a toxic metal that induces DNA single- and double-strand breaks (DSBs). Herein, we showed that PRDX1 interacts with ATM. PRDX1-deleted cells have reduced ATM, MRE11, and RAD50 protein levels, but not NBS1. In control cells treated with arsenite, we observed γH2AX foci formation due to arsenite-induced DSBs, and not from PRDX1-deleted cells. Arsenite caused profound depletion of ATM in PRDX1-deleted cells, suggesting that PRDX1 protects and stabilizes ATM required to form γH2AX foci. Importantly, arsenite pretreatment of PRDX1-deleted cells caused hypersensitivity to chemotherapeutic agents that generate DSBs. Analysis of a clinical cohort of ovarian cancers treated with platinum chemotherapy revealed that tumours with high PRDX1/high ATM or high PRDX1/high MRE11 expression manifested aggressive phenotypes and poor patient survival. The data suggest that PRDX1 can predict responses to chemotherapy, and targeting PRDX1 could be a viable strategy to improve the efficacy of platinum chemotherapy.

Indexed as

ArsenitesAtaxia Telangiectasia Mutated ProteinsDNA DamagePeroxiredoxinsAcid Anhydride HydrolasesCell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairDNA Repair EnzymesFemaleHistonesHumansMRE11 Homologue ProteinNuclear ProteinsAcid Anhydride HydrolasesarseniteArsenitesAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesH2AX protein, humanHistonesMRE11 Homologue ProteinMRE11 protein, humanNBN protein, humanNuclear ProteinsPeroxiredoxinsPRDX1 protein, humanRAD50 protein, humancell cyclehomologous recombinationprotein interactionprotein modificationredox signaling

Identifiers

PMID40387816
PMCPMC12088036

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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.