ArticleAutophagy2025
ADSL-produced fumarate increases BECN1 dimethylation to promote autophagy and liver tumor growth.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Metabolic regulation of calcium homeostasis via SERCA succination.Science advances · 2026Article
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Mitochondrial autophagy mechanism and berberine therapeutic target discovery in hepatocellular carcinoma based on single-cell and transcriptome analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- SIN3A promotes lung adenocarcinoma by repressing MIR22HG/Beclin1 axis-mediated autophagy and ferroptosis.European journal of medical research · 2026Article
- From organelles to therapy: rethinking combined hepatocellular-cholangiocarcinoma.Frontiers in cell and developmental biology · 2026Review
- JMJD5: a multifunctional regulator in development, homeostasis, and cancer.Frontiers in cell and developmental biology · 2026Review
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7 authors.
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Abstract
Cancer cells depend on the reprogramming of cell metabolism to constantly adapt metabolically to the tumor microenvironment. ADSL (adenylosuccinate lyase), a rate-limiting enzyme in de novo purine synthesis, is overexpressed in various cancer cells. However, whether ADSL functions in other oncogenic signaling is largely unknown. Here, our recent study shows that ADSL interacts with BECN1 (beclin 1) to regulate macroautophagy/autophagy upon lipid deprivation. Mechanistically, ADSL is phosphorylated at S140 by EIF2AK3/PERK (eukaryotic translation initiation factor 2 alpha kinase 3) in response to lipid deprivation, which enhances the association between ADSL and BECN1. ADSL-produced fumarate reduces the BECN1-associated KDM8 activity, leading to increased BECN1 K117 dimethylation. BECN1 K117 dimethylation inhibits its interaction with BCL2 to initiate autophagy. Targeting the ADSL-BECN1 axis by knock-in mutation or a cell-penetrating peptide inhibits autophagy and blunts liver tumor growth in mice. These findings broaden the physiological significance of ADSL in autophagy and liver tumor development.
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