ArticleNature metabolism2025
Hepatic gluconeogenesis and PDK3 upregulation drive cancer cachexia in flies and mice.
Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Host metadherin coordinates hepatic lipid metabolism and CD8Cell metabolism · 2026Article
- A Landscape ofBiology · 2026Review
- Gut-derived Unpaired-3 cytokine signaling promotes systemic hypoxia tolerance in Drosophila.Disease models & mechanisms · 2026Article
- Regulation and clinical manifestations of gluconeogenesis dysfunction.npj metabolic health and disease · 2026Review
- Lipid metabolism of hepatocyte-like cells supports intestinal tumor growth in Drosophila.Nature communications · 2026Article
- Article
- Credit to the Fruit Fly: How the Tiny Insect Lights Up Our Understanding of Human Disease.Insects · 2026Review
- Dual activation of cuproptosis and excessive autophagy by copper-bismuth metal-organic frameworks-loaded detachable microneedles in oral leukoplakia.Materials today. Bio · 2026Article
- Tumour-driven lipid accumulation in oenocytes reflects systemic lipid alterations.PLoS genetics · 2026Article
- Renal coenzyme A (CoA) production from VB5 fuels stem cell proliferation and tumor growth.Nature communications · 2026Article
- Phage display-mediated immuno-PCR to detect low-abundance secreted proteins inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Beyond Mice and Men: Alternative Vertebrate and Invertebrate Models in Cancer Biology.Annual review of cancer biology · 2026Article
- Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms.Nature communications · 2026Article
- Patient-derived organoid xenografts model esophageal cancer cachexia and enable assessment of anti-inflammatory drug repositioning.iScience · 2026Article
- The Drosophila proventriculus lacks stem cells but compensates for age-related cell loss via endoreplication-mediated cell growth.Nature communications · 2026Article
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- Allograft transplantation for Drosophila tumor metastasis studies.Disease models & mechanisms · 2025Article
- Hepatic ceramide synthesis links systemic inflammation to organelle dysfunction in cancer.bioRxiv : the preprint server for biology · 2025Article
- Cancer therapy and cachexia.The Journal of clinical investigation · 2025Review
- The roles of Cryptochrome-1: the circadian clock as a control point in cancer therapy.Journal of translational medicine · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
Cachexia, a severe wasting syndrome characterized by tumour-induced metabolic dysregulation, is a leading cause of death in people with cancer, yet its underlying mechanisms remain poorly understood. Here we show that a longitudinal full-body single-nuclei-resolution transcriptome analysis in a Drosophila model of cancer cachexia captures interorgan dysregulations. Our study reveals that the tumour-secreted interleukin-like cytokine Upd3 induces fat-body expression of Pepck1 and Pdk, key regulators of gluconeogenesis, disrupting glucose metabolism and contributing to cachexia. Similarly, in mouse cancer cachexia models, we observe IL-6-JAK-STAT-signalling-mediated induction of Pck1 and Pdk3 expression in the liver. Increased expression of these genes in fly, mouse, and human correlates with poor prognosis, and hepatic expression of Pdk3 emerges as a previously unknown mechanism contributing to metabolic dysfunction in cancer cachexia. This study highlights the conserved nature of tumour-induced metabolic disruptions and identifies potential therapeutic targets to mitigate cachexia in people with cancer.
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