ArticleCell2014
Acetate dependence of tumors.
Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 410 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
410 citing papers in PubMed, 2 syntheses or guidelines pooled it, 677 citations in OpenAlex.
- Aberrant Energy Metabolism in Tumors and Potential Therapeutic Targets.Genes, chromosomes & cancer · 2024Pooled it
- The role of lipid metabolic reprogramming in tumor microenvironment.Theranostics · 2023Pooled it
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Acetyl-CoA synthetase 2 maintains cytosolic acetyl-CoA homeostasis to preserve mitochondrial integrity and attenuate cardiac dysfunction under chronic β-adrenergic stress.Journal of molecular and cellular cardiology plus · 2026Article
- Article
- Carrier-free nanomodulators reprogramming acetate metabolism for cancer photo-immunotherapy via c-Myc inhibition-induced closed-loop regulatory circuit.Materials today. Bio · 2026Article
- Advances in Exercise-Mediated Regulation of the Gut Microbiota via the Muscle-Gut Axis: Implications for Tumor Immunity and Treatment Responses.Metabolites · 2026Review
- Precision metabolic therapy for propionic acidemia.Biochemical pharmacology · 2026Review
- ACSS2 is required for colorectal cancer progression and a druggable target for colorectal cancer treatment.iScience · 2026Article
- An EZH2-SREBP2 axis promotes cholesterol biosynthesis and represents a noncanonical vulnerability in tumorigenesis.Nature cell biology · 2026Article
- The interplay between lipid metabolism, cancer progression and anti-cancer immunity.Experimental & molecular medicine · 2026Review
- Fatty acids metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Clinical and experimental medicine · 2026Review
- Observational
- Article
- ACSS2 Suppresses Ferroptosis to Drive Breast Cancer Brain Metastasis.Cancer research · 2026Article
- Antitumor immunotoxin expression is enhanced by Escherichia coli csrB-promoter activity.Oncogene · 2026Article
- Ablation of ACSS2 drives alteration to cardiac and hepatic proteomic landscapes in a tissue- and sex-specific manner.Journal of proteomics · 2026Article
- Article
- Cold-Induced Serum Short-Chain Fatty Acids Act as Markers of Brown Adipose Tissue Metabolism in Humans.The Journal of clinical endocrinology and metabolism · 2026Article
- Acetyl-coenzyme A synthetase 2-mediated acetyl-coenzyme A accumulation promotes mitophagy and tumor growth via increased H3K27ac in hepatitis B virus-related hepatocellular carcinoma.Clinical and molecular hepatology · 2026Article
350 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Acetyl-CoA represents a central node of carbon metabolism that plays a key role in bioenergetics, cell proliferation, and the regulation of gene expression. Highly glycolytic or hypoxic tumors must produce sufficient quantities of this metabolite to support cell growth and survival under nutrient-limiting conditions. Here, we show that the nucleocytosolic acetyl-CoA synthetase enzyme, ACSS2, supplies a key source of acetyl-CoA for tumors by capturing acetate as a carbon source. Despite exhibiting no gross deficits in growth or development, adult mice lacking ACSS2 exhibit a significant reduction in tumor burden in two different models of hepatocellular carcinoma. ACSS2 is expressed in a large proportion of human tumors, and its activity is responsible for the majority of cellular acetate uptake into both lipids and histones. These observations may qualify ACSS2 as a targetable metabolic vulnerability of a wide spectrum of tumors.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.