Evidence map›Paper›PMID 41535921›Full record

ArticleCancer cell international2026

Ophiobolin A impacts mitochondrial redox biology in an epithelial-mesenchymal transition (EMT)-specific manner.

Haleigh N Parker, Yongfeng Tao, Jenna Tobin, Kayla L Haberman, Samantha Davis, Emily York, Alysia Martinez, Nobuyuki Matsumoto, Jaquelin Aroujo, Jun Hyoung Park and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell international, 2026. 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. Review
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

19 authors.

Haleigh N ParkerDepartment of Biology, Baylor University, TX, Waco, USA.
Yongfeng TaoScripps Research Institute, La Jolla, CA, USA.
Jenna TobinDepartment of Biology, Baylor University, TX, Waco, USA.
Kayla L HabermanDepartment of Biology, Baylor University, TX, Waco, USA.
Samantha DavisDepartment of Biology, Baylor University, TX, Waco, USA.
Emily YorkDepartment of Biology, Baylor University, TX, Waco, USA.
Alysia MartinezDepartment of Biology, Baylor University, TX, Waco, USA.
Nobuyuki MatsumotoDepartment of Chemistry and Biochemistry, Baylor University, Waco, TX, USA.
Jaquelin AroujoDepartment of Chemistry and Biochemistry, Baylor University, Waco, TX, USA.
Jun Hyoung ParkDepartment of Molecular and Human Genetics, Baylor College of Medicine, Waco, TX, USA.
Bernd ZechmannCenter for Microscopy and Imaging, Baylor University, Waco, TX, USA.
Benny Abraham KaipparettuDepartment of Molecular and Human Genetics, Baylor College of Medicine, Waco, TX, USA.
Angela BoariInstitute of Sciences and Food ProductionNational Research Council, Bari, Italy.
Christie M SayesDepartment of Environmental Science, Baylor University, Waco, TX, USA.
Antonio EvidenteInstitute of Biomolecular Sciences, National Research Council, Pozzuoli, Italy.
Alexander KornienkoDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX, USA.
Benjamin CravattScripps Research Institute, La Jolla, CA, USA.
Daniel RomoDepartment of Chemistry and Biochemistry, Baylor University, Waco, TX, USA.
Joseph H TaubeDepartment of Biology, Baylor University, TX, Waco, USA. Joseph_Taube@baylor.edu.

Funding

Chemical Proteomic Platforms for Radically Expanding Cancer DruggabilityR35CA231991 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI BENJAMIN F CRAVATT · 2018 to 2026
$9.5M
Pharmacophore-Directed  Retrosynthesis Applied to Bioactive Natural Products Informing Mechanism of Action StudiesR35GM134910 · NIGMS · BAYLOR UNIVERSITY · PI DANIEL ROMO · 2020 to 2026
$2.7M
Cancer Prevention and Research Institute of Texas RP180771NCI NIH HHS CA231991NCI NIH HHS R35 CA231991NIGMS NIH HHS GM134910NIGMS NIH HHS R35 GM134910
6 · The paper itself

Abstract

Breast cancer progression is facilitated by the epithelial to mesenchymal transition (EMT), generating cancer cells with enhanced metastatic capacity and resistance to chemotherapeutics. The fungus-derived sesterterpenoid natural produce compound, ophiobolin A (OpA), possesses nanomolar cytotoxic activity and a high therapeutic index, although its molecular targets and mechanism of action are not well characterized. Herein, we utilized a model of mammary epithelial cells and breast cancer cell lines with and without EMT features to characterize the mechanism of selectivity towards EMT(+) cells by OpA. Proteins interacting with OpA in EMT(+) cells, including mitochondrial glutathione transporter SLC25A40, were identified through via mass spectrometry. We utilized trans-mitochondrial cybrids to determine that mitochondria mediate sensitivity to OpA. Furthermore, we report effects on glycolysis, oxidative metabolism, and disruption of metabolite abundance in the TCA cycle. Antioxidant mechanisms are activated by OpA in EMT(+) cells via the NRF2-ARE pathway, verified by decreased cytotoxicity in EMT(+) cells pretreated with the NRF2 activator CDDO. Collectively, we conclude that OpA selectivity toward EMT is mediated by the mitochondria, and at sub-cytotoxic levels, generates a metabolic shift leading to cell death countered by antioxidant mechanisms.

Indexed as

Epithelial-mesenchymal transitionMitochondriaOphiobolin ASLC25A40

Identifiers

PMID41535921
PMCPMC12888505

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.