Acquired resistance to jadomycin B in human triple-negative breast cancer cells is associated with increased cyclooxygenase-2 expression.

Brendan T McKeown, Brandon Groves, David L Jakeman, Kerry B Goralski

Abstract read

In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in

0citing 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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

4 authors.

Brendan T McKeownDepartment of Pharmacology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Beatrice Hunter Cancer Research Institute, Halifax, Nova Scotia, Canada.

Brandon GrovesDepartment of Chemistry, Faculty of Sciences, Dalhousie University, Halifax, Nova Scotia, Canada.

David L JakemanDepartment of Chemistry, Faculty of Sciences, Dalhousie University, Halifax, Nova Scotia, Canada; College of Pharmacy, Faculty of Health, Dalhousie University, Halifax, Nova Scotia, Canada.

Kerry B GoralskiDepartment of Pharmacology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Beatrice Hunter Cancer Research Institute, Halifax, Nova Scotia, Canada; College of Pharmacy, Faculty of Health, Dalhousie University, Halifax, Nova Scotia, Canada; Division of Pediatric Hematology and Oncology, Department of Pediatrics, IWK Health Centre, Halifax, Nova Scotia, Canada. Electronic address: kerry.goralski@dal.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Jadomycin B, produced by the soil bacterium Streptomyces venezuelae ISP5230, induces cytotoxicity in human breast cancer cells in vitro and has antitumoral effects in animal models. In models of multidrug-resistant, triple-negative breast cancer, jadomycin B has shown promise as it is not a substrate of ABCB1 and ABCG2 drug efflux transporters. The generation of reactive oxygen species and inhibition of topoisomerases are potential mechanisms of jadomycin B-mediated DNA damage and apoptosis. However, the mechanisms of jadomycin B's anticancer activity have not been fully elucidated. By gradually exposing MDA-MB-231 triple-negative human breast cancer cells to jadomycin B, we hypothesized that resistance could be selected to further understand jadomycin B's pharmacological mechanisms. A 3-fold increase in the jadomycin B IC

Indexed as

Cyclooxygenase 2Drug Resistance, NeoplasmIsoquinolinesNaphthoquinonesTriple Negative Breast NeoplasmsAntineoplastic AgentsCell Line, TumorFemaleHumansAntineoplastic AgentsCyclooxygenase 2IsoquinolinesNaphthoquinonesPTGS2 protein, humanATP-binding cassette transportBreast cancerCyclooxygenaseJadomycinMultidrug resistanceTopoisomerase

Identifiers

PMID40253988

DOI10.1016/j.jpet.2025.103565

PMCPMC12163490

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LicenceCC BY

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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.