Evidence map›Paper›PMID 42673947›Full record

ArticleCell reports. Medicine2026

Lysyl oxidase inhibition disrupts mitochondrial homeostasis to create vulnerability to ferroptosis in TNBC.

Ozge Saatci, Burge Ulukan, Metin Cetin, Hellen Kuasne, Constanza Martinez, Elif Percin, Natalia Oleinik, Matthew T Savoca, Ali Nehme, Aldo Hernández-Corchado and 21 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 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

31 authors.

Ozge SaatciDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Burge UlukanDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Metin CetinDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Hellen KuasneRosalind and Morris Goodman Cancer Institute, McGill University, Montréal, QC H3A 1A3, Canada.
Constanza MartinezRosalind and Morris Goodman Cancer Institute, McGill University, Montréal, QC H3A 1A3, Canada; Department of Radiation Oncology, McGill University Health Centre, Montréal, QC H4A 3J1, Canada.
Elif PercinDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Natalia OleinikDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Matthew T SavocaDepartment of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Ali NehmeDepartment of Human Genetics, McGill University, Montréal, QC H3A 0G1, Canada.
Aldo Hernández-CorchadoDepartment of Human Genetics, McGill University, Montréal, QC H3A 0G1, Canada.
Evelyn ZavackyDepartment of Human Genetics, McGill University, Montréal, QC H3A 0G1, Canada.
Kukkamudi SreenivasDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, Columbia, SC 29208, USA.
Abdol H RezaeianDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, Columbia, SC 29208, USA.
Jennifer R BethardDepartment of Pharmacology & Immunology, Proteomics Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Jean-Sebastien AnomaDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Ozlem Sener SahinDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Adriana Aguilar-MahechaLady Davis Institute, Jewish General Hospital, McGill University, Montréal, QC H3T 1E2, Canada.
Marguerite BuchananLady Davis Institute, Jewish General Hospital, McGill University, Montréal, QC H3T 1E2, Canada.
Mertkaya ArasDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, Columbia, SC 29208, USA.
Genevieve DeBloisInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, QC H3T 1J4, Canada; Faculty of Pharmacy, Université de Montréal, Montréal, QC H3T 1J4, Canada.
Mark BasikLady Davis Institute, Jewish General Hospital, McGill University, Montréal, QC H3T 1E2, Canada.
Elizabeth G HillDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Lauren E BallDepartment of Pharmacology & Immunology, Proteomics Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Chintada Nageswara RaoDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, Columbia, SC 29208, USA.
Campbell McInnesDepartment of Drug Discovery and Biomedical Sciences, University of South Carolina, Columbia, SC 29208, USA.
Yasser RiazalhosseiniDepartment of Human Genetics, McGill University, Montréal, QC H3A 0G1, Canada; Victor Phillip Dahdaleh Institute of Genomic Medicine at McGill University, Montréal, QC H3A 0G1, Canada.
Hamed S NajafabadiDepartment of Human Genetics, McGill University, Montréal, QC H3A 0G1, Canada.
John J LemastersDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA; Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Besim OgretmenDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Morag ParkRosalind and Morris Goodman Cancer Institute, McGill University, Montréal, QC H3A 1A3, Canada; Department of Biochemistry, McGill University, Montréal, QC H3A 0G1, Canada; Department of Oncology, McGill University, Montréal, QC H3A 0G1, Canada.
Ozgur SahinDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA. Electronic address: sahin@musc.edu.

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI John J Lemasters · 2009 to 2026
$42.7M
SOUTH CAROLINA COBRE IN OXIDANTS, REDOX BALANCE AND STRESS SIGNALINGP20GM103542 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LEMASTERS, JOHN J · 2012 to 2020
$20.2M
Ceramide Signaling in the Regulation of Head & Neck Cancer Cell Death and TherapyR01DE016572 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI OGRETMEN, BESIM · 2005 to 2025
$7.4M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CROUCH, ROSALIE K · 2002 to 2002
$2.0M
Overcoming chemoresistance in triple negative breast cancerR01CA267101 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI Ozgur Sahin · 2022 to 2026
$1.8M
Inhibiting tumor growth and metastasis in highly aggressive breast cancers with centrosome amplificationR01CA251374 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI SAHIN, OZGUR · 2021 to 2025
$1.7M
Quadrupole Orbitrap Hybrid Mass Spectrometer for ProteomicsS10OD028692 · OD · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BALL, LAUREN ELIZABETH · 2021 to 2021
$773k
Confocal/Multiphoton Microscope UpgradeS10OD018113 · OD · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LEMASTERS, JOHN J · 2015 to 2015
$570k
NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA251374NCI NIH HHS R01 CA267101NCRR NIH HHS C06 RR015455NIDCR NIH HHS R01 DE016572NIGMS NIH HHS P20 GM103542NIH HHS S10 OD018113NIH HHS S10 OD028692
6 · The paper itself

Abstract

High metabolic heterogeneity and plasticity of triple-negative breast cancer (TNBC) contribute to therapy resistance, necessitating identification of therapeutic vulnerabilities. Here, we identify non-canonical functions of the extracellular matrix (ECM) remodeler, lysyl oxidase (LOX), in regulating glucose metabolism and mitochondrial homeostasis and show that inhibiting LOX generates targetable vulnerability to ferroptosis. Mechanistically, LOX interacts with PARKIN and its upstream kinase PINK1, which we identified as a substrate of LOX. LOX-mediated PINK1 oxidation suppresses PARKIN phosphorylation, stabilizing hypoxia-inducible factor 1-alpha (HIF-1α) and increasing glycolysis. Concomitantly, LOX inhibits PARKIN-mediated mitophagy and maintains mitochondria-ER contacts through VDAC1 stabilization, while the LOX-HSP90 complex promotes mitochondrial Ca

Indexed as

FerroptosisHomeostasisMitochondriaProtein-Lysine 6-OxidaseTriple Negative Breast NeoplasmsAnimalsCell Line, TumorFemaleGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitMiceMitophagyHypoxia-Inducible Factor 1, alpha SubunitProtein-Lysine 6-OxidaseDHODHferroptosisglucose metabolismLOXlysyl oxidaseMERCSmitochondria-ER contactsmitophagyTNBC

Identifiers

PMID42673947
PMCPMC13589490

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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.