ArticleNature cancer2025
Selective deficiency of mitochondrial respiratory complex I subunits Ndufs4/6 causes tumor immunogenicity.
Article in Nature cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- LARS2 reprograms mitochondrial metabolism and epigenetically upregulates MHC-I to boost antitumor immunity in nasopharyngeal carcinoma.Journal for immunotherapy of cancer · 2026Article
- First Total-Body Kinetics Study ofJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026Article
- Metabolites as signalling molecules in the tumour immune microenvironment.Nature reviews. Immunology · 2026Review
- The metabolic plasticity of cancer stem cells: bidirectional crosstalk with organ-resident cells.Experimental & molecular medicine · 2026Review
- Article
- Mitochondrial metabolism and signaling direct dendritic cell function in antitumor immunity.Science (New York, N.Y.) · 2026Article
- Machine learning-driven identification of shared and disease-specific mitochondria-related genes in COPD, NSCLC, and NSCLC with COPD.iScience · 2026Article
- Loss of ten-eleven translocation 2 (TET2) facilitates aggressive behaviour in cutaneous melanoma by inducing peroxisome proliferator-activated receptor-γ coactivator 1α expression and oxidative phosphorylation.The British journal of dermatology · 2026Article
- Integrative machine learning-driven prognosis and immunotherapy stratification via lactylation-associated gene in ovarian cancer.NPJ precision oncology · 2025Article
- Metabolic reprogramming in diffuse intrinsic pontine gliomas (DIPG): dual inhibition of mitochondrial oxidative phosphorylation and lactate metabolism to enhance anti-tumor and radiosensitizing effects in DIPG cells.Cancer & metabolism · 2025Article
- Mitochondrial Proteins as Exosomal Cargo: New Breast Cancer Biomarkers & Crucial Players in Carcinogenesis?Molecules (Basel, Switzerland) · 2025Article
- The RNA-Binding Protein RBMX Mediates the Immunosuppressive Microenvironment of Osteosarcoma by Regulating CD8Cancers · 2025Article
- Multi-omic insights into mitochondrial dysfunction and prostatic disease: evidence from transcriptomics, proteomics, and methylomics.Frontiers in genetics · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Cancer cells frequently rewire their metabolism to support proliferation and evade immune surveillance, but little is known about metabolic targets that could increase immune surveillance. Here we show a specific means of mitochondrial respiratory complex I (CI) inhibition that improves tumor immunogenicity and sensitivity to immune checkpoint blockade (ICB). Targeted genetic deletion of either Ndufs4 or Ndufs6, but not other CI subunits, induces an immune-dependent growth attenuation in melanoma and breast cancer models. We show that deletion of Ndufs4 induces expression of the major histocompatibility complex (MHC) class I co-activator Nlrc5 and antigen presentation machinery components, most notably H2-K1. This induction of MHC-related genes is driven by a pyruvate dehydrogenase-dependent accumulation of mitochondrial acetyl-CoA, which leads to an increase in histone H3K27 acetylation within the Nlrc5 and H2-K1 promoters. Taken together, this work shows that selective CI inhibition restricts tumor growth and that specific targeting of Ndufs4 or Ndufs6 increases T cell surveillance and ICB responsiveness.
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