ArticleThe EMBO journal2022
Ketogenic HMG-CoA lyase and its product β-hydroxybutyrate promote pancreatic cancer progression.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 66 citations in OpenAlex.
- Ketogenic Diet as an Adjuvant in Epithelial Cancers: Mechanisms, Model Systems, and Translational Opportunities.Cancers · 2026Review
- Article
- Amplification of MED30 at chromosome 8q24 reprograms MYC binding to low-affinity oncogenic enhancers in cancer cells.Cell reports · 2026Article
- β-Hydroxybutyrate Inhibits Angiogenesis, Suppresses Non-Small Cell Lung Cancer Growth, and Enhances Gemcitabine Antitumor Activity.International journal of molecular sciences · 2026Article
- Ketone body metabolism activates the immune response againstCell insight · 2026Article
- Metabolic Salvage and Acyl-chain Remodeling Support Glycosphingolipid Synthesis within the PDAC Tumor Microenvironment.bioRxiv : the preprint server for biology · 2026Article
- ZNF460 inhibits HMGCL and promotes PI3K pathway in colon cancer.Translational cancer research · 2026Article
- TIGAR maintains intestinal epithelial regeneration by stabilizing HMGCL and promoting β-catenin β-hydroxybutyrylation in burn-induced sepsis.Cell death & disease · 2026Article
- Ketone bodies in kidney diseases: novel insights.Frontiers in immunology · 2026Review
- Integrative analysis of pancreatic microbiota and metabolome in patients with pancreatic ductal adenocarcinoma.Scientific reports · 2025Article
- The extracellular matrix drives guanylate production and protects pancreatic cancer cells from oxaliplatin-induced DNA damage.Science advances · 2025Article
- Identification of potential biomarkers associated with mitochondrial oxidative stress in idiopathic pulmonary arterial hypertension via bioinformatic and experimental analysis.Scientific reports · 2025Article
- Identification of EFNA3 as candidate prognosis marker and potential therapeutic target for adrenocortical carcinoma.Oncology letters · 2025Article
- An alternative route for β-hydroxybutyrate metabolism supports cytosolic acetyl-CoA synthesis in cancer cells.Nature metabolism · 2025Article
- The Microbiota-Diet-Immunity Axis in Cancer Care: From Prevention to Treatment Modulation and Survivorship.Nutrients · 2025Review
- Circulating proteins and metabolites panel for noninvasive preoperative diagnosis of epithelial ovarian cancer.BMC medicine · 2025Article
- ACSS2 coupled with KAT7 regulates histone β-hydroxybutyrylation to enhance transcription.Science advances · 2025Article
- β-Hydroxybutyrate promotes cancer metastasis through β-hydroxybutyrylation-dependent stabilization of Snail.Nature communications · 2025Article
- Ketogenic diet prevents obesity-associated pancreatic cancer independent of weight loss and induces pancreatic metabolic reprogramming.bioRxiv : the preprint server for biology · 2025Article
- Ketomimetic nutrients remodel the glycocalyx and trigger a metabolic defense in breast cancer cells.Cancer & metabolism · 2025Article
Corrections and comments
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Authors and funding
23 authors at 3 institutions in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDA) tumor cells are deprived of oxygen and nutrients and therefore must adapt their metabolism to ensure proliferation. In some physiological states, cells rely on ketone bodies to satisfy their metabolic needs, especially during nutrient stress. Here, we show that PDA cells can activate ketone body metabolism and that β-hydroxybutyrate (βOHB) is an alternative cell-intrinsic or systemic fuel that can promote PDA growth and progression. PDA cells activate enzymes required for ketogenesis, utilizing various nutrients as carbon sources for ketone body formation. By assessing metabolic gene expression from spontaneously arising PDA tumors in mice, we find HMG-CoA lyase (HMGCL), involved in ketogenesis, to be among the most deregulated metabolic enzymes in PDA compared to normal pancreas. In vitro depletion of HMGCL impedes migration, tumor cell invasiveness, and anchorage-independent tumor sphere compaction. Moreover, disrupting HMGCL drastically decreases PDA tumor growth in vivo, while βOHB stimulates metastatic dissemination to the liver. These findings suggest that βOHB increases PDA aggressiveness and identify HMGCL and ketogenesis as metabolic targets for limiting PDA progression.
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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.