Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer

Abstract Lactate dehydrogenase B (LDHB) fuels oxidative cancer cell metabolism by converting lactate to pyruvate. This study uncovers LDHB’s role in countering mitochondria-associated ferroptosis independently of lactate’s function as a carbon source. LDHB silencing alters mitochondrial morphology,...

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Main Authors: Haibin Deng, Liang Zhao, Huixiang Ge, Yanyun Gao, Yan Fu, Yantang Lin, Mojgan Masoodi, Tereza Losmanova, Michaela Medová, Julien Ott, Min Su, Wenxiang Wang, Ren-Wang Peng, Patrick Dorn, Thomas Michael Marti
Format: Article
Language:English
Published: Nature Portfolio 2025-03-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-57906-3
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author Haibin Deng
Liang Zhao
Huixiang Ge
Yanyun Gao
Yan Fu
Yantang Lin
Mojgan Masoodi
Tereza Losmanova
Michaela Medová
Julien Ott
Min Su
Wenxiang Wang
Ren-Wang Peng
Patrick Dorn
Thomas Michael Marti
author_facet Haibin Deng
Liang Zhao
Huixiang Ge
Yanyun Gao
Yan Fu
Yantang Lin
Mojgan Masoodi
Tereza Losmanova
Michaela Medová
Julien Ott
Min Su
Wenxiang Wang
Ren-Wang Peng
Patrick Dorn
Thomas Michael Marti
author_sort Haibin Deng
collection DOAJ
description Abstract Lactate dehydrogenase B (LDHB) fuels oxidative cancer cell metabolism by converting lactate to pyruvate. This study uncovers LDHB’s role in countering mitochondria-associated ferroptosis independently of lactate’s function as a carbon source. LDHB silencing alters mitochondrial morphology, causes lipid peroxidation, and reduces cancer cell viability, which is potentiated by the ferroptosis inducer RSL3. Unlike LDHA, LDHB acts in parallel with glutathione peroxidase 4 (GPX4) and dihydroorotate dehydrogenase (DHODH) to suppress mitochondria-associated ferroptosis by decreasing the ubiquinone (coenzyme Q, CoQ) to ubiquinol (CoQH2) ratio. Indeed, supplementation with mitoCoQH2 (mitochondria-targeted analogue of CoQH2) suppresses mitochondrial lipid peroxidation and cell death after combined LDHB silencing and RSL3 treatment, consistent with the presence of LDHB in the cell fraction containing the mitochondrial inner membrane. Addressing the underlying molecular mechanism, an in vitro NADH consumption assay with purified human LDHB reveals that LDHB catalyzes the transfer of reducing equivalents from NADH to CoQ and that the efficiency of this reaction increases by the addition of lactate. Finally, radiation therapy induces mitochondrial lipid peroxidation and reduces tumor growth, which is further enhanced when combined with LDHB silencing. Thus, LDHB-mediated lactate oxidation drives the CoQ-dependent suppression of mitochondria-associated ferroptosis, a promising target for combination therapies.
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spelling doaj-art-71dde92752824cfe97190c44dd71465e2025-08-20T02:56:09ZengNature PortfolioNature Communications2041-17232025-03-0116111710.1038/s41467-025-57906-3Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancerHaibin Deng0Liang Zhao1Huixiang Ge2Yanyun Gao3Yan Fu4Yantang Lin5Mojgan Masoodi6Tereza Losmanova7Michaela Medová8Julien Ott9Min Su10Wenxiang Wang11Ren-Wang Peng12Patrick Dorn13Thomas Michael Marti142nd Department of Thoracic Surgery, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South UniversityDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalInstitute of Clinical Chemistry, Inselspital, Bern University HospitalInstitute of Tissue Medicine and Pathology, ITMP, University of BernHunan Clinical Medical Research Center of Accurate Diagnosis and Treatment for esophageal carcinoma, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South UniversityDepartment of Radiation Oncology, Inselspital, Bern University Hospital2nd Department of Thoracic Surgery, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University2nd Department of Thoracic Surgery, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South UniversityDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalDepartment of General Thoracic Surgery, Inselspital, Bern University HospitalAbstract Lactate dehydrogenase B (LDHB) fuels oxidative cancer cell metabolism by converting lactate to pyruvate. This study uncovers LDHB’s role in countering mitochondria-associated ferroptosis independently of lactate’s function as a carbon source. LDHB silencing alters mitochondrial morphology, causes lipid peroxidation, and reduces cancer cell viability, which is potentiated by the ferroptosis inducer RSL3. Unlike LDHA, LDHB acts in parallel with glutathione peroxidase 4 (GPX4) and dihydroorotate dehydrogenase (DHODH) to suppress mitochondria-associated ferroptosis by decreasing the ubiquinone (coenzyme Q, CoQ) to ubiquinol (CoQH2) ratio. Indeed, supplementation with mitoCoQH2 (mitochondria-targeted analogue of CoQH2) suppresses mitochondrial lipid peroxidation and cell death after combined LDHB silencing and RSL3 treatment, consistent with the presence of LDHB in the cell fraction containing the mitochondrial inner membrane. Addressing the underlying molecular mechanism, an in vitro NADH consumption assay with purified human LDHB reveals that LDHB catalyzes the transfer of reducing equivalents from NADH to CoQ and that the efficiency of this reaction increases by the addition of lactate. Finally, radiation therapy induces mitochondrial lipid peroxidation and reduces tumor growth, which is further enhanced when combined with LDHB silencing. Thus, LDHB-mediated lactate oxidation drives the CoQ-dependent suppression of mitochondria-associated ferroptosis, a promising target for combination therapies.https://doi.org/10.1038/s41467-025-57906-3
spellingShingle Haibin Deng
Liang Zhao
Huixiang Ge
Yanyun Gao
Yan Fu
Yantang Lin
Mojgan Masoodi
Tereza Losmanova
Michaela Medová
Julien Ott
Min Su
Wenxiang Wang
Ren-Wang Peng
Patrick Dorn
Thomas Michael Marti
Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer
Nature Communications
title Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer
title_full Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer
title_fullStr Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer
title_full_unstemmed Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer
title_short Ubiquinol-mediated suppression of mitochondria-associated ferroptosis is a targetable function of lactate dehydrogenase B in cancer
title_sort ubiquinol mediated suppression of mitochondria associated ferroptosis is a targetable function of lactate dehydrogenase b in cancer
url https://doi.org/10.1038/s41467-025-57906-3
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