ArticleCommunications biology2025
OXCT1 promotes triple negative breast cancer immune escape via modulating succinylation modification of PGK1.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- KMT5a-Mediated IRF3 Stabilization Enhances Macrophage Chemotaxis and Renal Fibrosis Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- A succinylation-based classifier predicts chemotherapy response in prostate cancer and reveals KAT2A as a therapeutic target.Clinical and translational medicine · 2026Article
- A photodynamically activated nanoplatform relieves glucose-driven immunosuppression to potentiate STING immunotherapy in triple-negative breast cancer.Materials today. Bio · 2026Article
- Decoding the crosstalk between ubiquitination and other post-translational modifications in cancer immunity: from mechanisms to clinical prospects.NPJ precision oncology · 2026Review
- A computational framework integrating multi-omics and machine learning for identifying glycolytic gene markers in breast cancer.Discover oncology · 2026Article
- Succinylation: A Functional Nexus Between Metabolic Reprogramming and Epigenetic Modifications in Cancer.Molecules (Basel, Switzerland) · 2026Review
- A Cori cycle-related gene signature predicts prognosis, immune microenvironment, and drug response in breast cancer.Translational cancer research · 2026Article
- Succinylation: novel molecular mechanisms and prospects for targeted therapy in liver diseases.Frontiers in molecular biosciences · 2026Review
- PARK2-Mediated PGK1 Degradation Suppresses Partial Epithelial-Mesenchymal Transition and Metastasis in Triple-Negative Breast Cancer.Oncology research · 2026Article
- Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies.Clinical epigenetics · 2025Review
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6 authors.
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Abstract
Immunotherapy has made a breakthrough in triple negative breast cancer (TNBC). The aim of this study is to investigate the specific role and regulatory mechanism of 3-oxoacid CoA-transferase 1 (OXCT1) in influencing TNBC growth and immune escape induced by aerobic glycolysis. OXCT1-induced enhancement of TNBC cell proliferation and PD-L1 expression is reversed by 2-DG. After interference with OXCT1 in TNBC patient-derived organoids (PDOs), tumor cell proliferation and lactic acid secretion are attenuated, and T-cell killing is enhanced. OXCT1 correlates with phosphoglycerate kinase 1 (PGK1) protein expression in clinical TNBC samples. In vitro overexpression of OXCT1 has no significant effect on PGK1 mRNA expression, but increases the succinylation level of PGK1 K146 and its protein stability, while decreasing its ubiquitination. The H4K20me1 level in the OXCT1 promoter region is increased in TNBC tissues, and in vitro lysine methyltransferase 5 A (KMT5A) overexpression increases the H4K20me1 level in the OXCT1 promoter region to promote OXCT1 expression. In conclusion, OXCT1 interference reverses the KMT5A-induced enhancement of TNBC cell viability, proliferation, and PD-L1 expression. KMT5A promotes OXCT1 expression through histone methylation, and OXCT1 increases PGK1 protein stability through succinylation modification, thereby promoting aerobic glycolysis and immune escape in TNBC.
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