Evidence map›Paper›PMID 31842863›Full record

ArticleBMC cancer2019

ROS as a novel indicator to predict anticancer drug efficacy.

Tarek Zaidieh, James R Smith, Karen E Ball, Qian An

Abstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing 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

64 citing papers in PubMed.

  1. Article
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  7. Ring-fused chlorin-enhanced photodynamic therapy for effective cell death induction in endometrial cancer.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
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  18. Impact of anthracycline-based chemotherapy on RB1 gene methylation in peripheral blood leukocytes and biomarkers of oxidative stress and inflammation in sarcoma patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  19. Review
  20. Review

4 more citing papers are in PubMed but not listed here.

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

4 authors.

Tarek ZaidiehSchool of Pharmacy and Biomedical Sciences, Institute of Biological and Biomedical Sciences, University of Portsmouth, Portsmouth, PO1 2DT, UK. tarek.zaidieh@port.ac.uk.
James R SmithSchool of Pharmacy and Biomedical Sciences, Institute of Biological and Biomedical Sciences, University of Portsmouth, Portsmouth, PO1 2DT, UK.
Karen E BallSchool of Pharmacy and Biomedical Sciences, Institute of Biological and Biomedical Sciences, University of Portsmouth, Portsmouth, PO1 2DT, UK.
Qian AnSchool of Pharmacy and Biomedical Sciences, Institute of Biological and Biomedical Sciences, University of Portsmouth, Portsmouth, PO1 2DT, UK. qian.an@port.ac.uk.ORCID http://orcid.org/0000-0003-1772-7268

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondria are considered a primary intracellular site of reactive oxygen species (ROS) generation. Generally, cancer cells with mitochondrial genetic abnormalities (copy number change and mutations) have escalated ROS levels compared to normal cells. Since high levels of ROS can trigger apoptosis, treating cancer cells with low doses of mitochondria-targeting / ROS-stimulating agents may offer cancer-specific therapy. This study aimed to investigate how baseline ROS levels might influence cancer cells' response to ROS-stimulating therapy.

methodsFour cancer and one normal cell lines were treated with a conventional drug (cisplatin) and a mitochondria-targeting agent (dequalinium chloride hydrate) separately and jointly. Cell viability was assessed and drug combination synergisms were indicated by the combination index (CI). Mitochondrial DNA copy number (mtDNAcn), ROS and mitochondrial membrane potential (MMP) were measured, and the relative expression levels of the genes and proteins involved in ROS-mediated apoptosis pathways were also investigated.

resultsOur data showed a correlation between the baseline ROS level, mtDNAcn and drug sensitivity in the tested cells. Synergistic effect of both drugs was also observed with ROS being the key contributor in cell death.

conclusionsOur findings suggest that mitochondria-targeting therapy could be more effective compared to conventional treatments. In addition, cancer cells with low levels of ROS may be more sensitive to the treatment, while cells with high levels of ROS may be more resistant. Doubtlessly, further studies employing a wider range of cell lines and in vivo experiments are needed to validate our results. However, this study provides an insight into understanding the influence of intracellular ROS on drug sensitivity, and may lead to the development of new therapeutic strategies to improve efficacy of anticancer therapy.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell SurvivalCisplatinDequaliniumFemaleHumansMaleMembrane Potential, MitochondrialMitochondriaNeoplasmsPrognosisReactive Oxygen SpeciesTreatment OutcomeCisplatinDequaliniumReactive Oxygen SpeciesCancer biomarkerCisplatinDequalinium chloride hydrateDrug sensitivityReactive oxygen species

Identifiers

PMID31842863
PMCPMC6916036

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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.