ArticleCell reports2024
ACSS1-dependent acetate utilization rewires mitochondrial metabolism to support AML and melanoma tumor growth and metastasis.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Metabolites and cancer metastasis.Oncogene · 2026Review
- Article
- BPGM as an intrinsic brake to constrain metastasis through phospho-epigenetic-mediated carnitine biosynthesis suppression.Neoplasia (New York, N.Y.) · 2026Article
- Gut Microbiota Alterations in Myelodysplastic Neoplasms Are Associated With Immune Dysfunction and the Therapeutic Mechanism of Hypomethylating Agents.Cancer medicine · 2026Article
- An acetylation-dependent switch underlies host disease tolerance during streptococcal infection.Scientific reports · 2026Article
- Targeting glycerophospholipid biosynthesis overcomes chemoresistance driven by SLFN11 loss in Ewing sarcoma.Cell death & disease · 2026Article
- Review
- Metabolic reprogramming as a driver of immune escape in melanoma: implications for immunotherapy.Frontiers in immunology · 2026Review
- Short-chain fatty acids in the tumor microenvironment: from molecular mechanisms to cancer therapy.Theranostics · 2026Review
- Microbiome dysbiosis and chemotherapy resistance in acute myeloid leukemia (AML).NPJ biofilms and microbiomes · 2025Review
- ACSS1 co-opts acetyl-CoA metabolism to drive DNA repair and undermine radiotherapy efficacy in breast cancer.Cell death & disease · 2025Article
- Extracellular vesicles derived from pro-inflammatory M1 macrophages induce an inflammatory and invasive phenotype in melanoma cells.Cell communication and signaling : CCS · 2025Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- Metabolic reprogramming in melanoma therapy.Cell death discovery · 2025Review
- High-content stimulated Raman pathology imaging and transcriptomics reveal leukemia subtype-specific lipid metabolic heterogeneity.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Cancer cells often use alternative nutrient sources to support their metabolism and proliferation. One important alternative nutrient source for many cancers is acetate. Acetate is metabolized into acetyl-coenzyme A (CoA) by acetyl-CoA synthetases 1 and 2 (ACSS1 and ACSS2), which are found in the mitochondria and cytosol, respectively. We show that ACSS1 and ACSS2 are differentially expressed in cancer. Melanoma, breast cancer, and acute myeloid leukemia cells expressing ACSS1 readily use acetate for acetyl-CoA biosynthesis and to fuel mitochondrial metabolism. ACSS1-dependent acetate metabolism decreases the relative contributions of glucose and glutamine to the tricarboxylic acid (TCA) cycle and alters the pentose phosphate pathway and redox state of cancer cells. ACSS1 knockdown decreases acute myeloid leukemia burden in vivo and inhibits melanoma tumor and metastatic growth. Our study highlights a key role for ACSS1-dependent acetate metabolism for cancer growth, raising the potential for ACSS1-targeting therapies in cancer.
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