ArticleCell reports2024
ALDH1A3-acetaldehyde metabolism potentiates transcriptional heterogeneity in melanoma.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
What it found
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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.
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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.
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Who cites it
11 citing papers in PubMed.
- ALDH1B1 promotes mitochondrial γ-butyrobetaine biosynthesis and fatty acid oxidation in colorectal cancer.bioRxiv : the preprint server for biology · 2026Article
- Host eicosanoid signals define a granuloma fibroblast population that coordinates mycobacterial containment.Cell host & microbe · 2026Article
- BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Molecular biomedicine · 2026Review
- Local acetyl-CoA metabolism and acetate recycling as epigenetic regulators of chromatin dynamics.FEMS yeast research · 2026Review
- LINC01116 promotes nascent protein synthesis and cellular stemness through the miR-432-5p/FKBP7/14 regulatory axis in melanoma.Scientific reports · 2025Article
- Article
- ACSS2 and metabolic diseases: from lipid metabolism to therapeutic target.Lipids in health and disease · 2025Review
- The Significance of Aldehyde Dehydrogenase 1 in Cancers.International journal of molecular sciences · 2024Review
- Cancer drug-tolerant persister cells: from biological questions to clinical opportunities.Nature reviews. Cancer · 2024Review
- Melanocyte lineage dynamics in development, growth and disease.Development (Cambridge, England) · 2024Review
- The Synergistic and Opposing Roles of ω-Fatty Acid Hydroxylase (Genome biology & molecular genetics · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
19 authors.
Funding
Abstract
Cancer cellular heterogeneity and therapy resistance arise substantially from metabolic and transcriptional adaptations, but how these are interconnected is poorly understood. Here, we show that, in melanoma, the cancer stem cell marker aldehyde dehydrogenase 1A3 (ALDH1A3) forms an enzymatic partnership with acetyl-coenzyme A (CoA) synthetase 2 (ACSS2) in the nucleus to couple high glucose metabolic flux with acetyl-histone H3 modification of neural crest (NC) lineage and glucose metabolism genes. Importantly, we show that acetaldehyde is a metabolite source for acetyl-histone H3 modification in an ALDH1A3-dependent manner, providing a physiologic function for this highly volatile and toxic metabolite. In a zebrafish melanoma residual disease model, an ALDH1-high subpopulation emerges following BRAF inhibitor treatment, and targeting these with an ALDH1 suicide inhibitor, nifuroxazide, delays or prevents BRAF inhibitor drug-resistant relapse. Our work reveals that the ALDH1A3-ACSS2 couple directly coordinates nuclear acetaldehyde-acetyl-CoA metabolism with specific chromatin-based gene regulation and represents a potential therapeutic vulnerability in melanoma.
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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 OpenQuestion graph.