ArticleNature cell biology2021
Tumour-derived Dilp8/INSL3 induces cancer anorexia by regulating feeding neuropeptides via Lgr3/8 in the brain.
Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 81 citations in OpenAlex.
- A Drosophila tumor model identifies a conserved Upd-JAK/STAT-Akh signaling axis associated with metabolic changes in cancer cachexia.Disease models & mechanisms · 2026Article
- Sexual identity of Akh neurons shapes Nucb1-dependent metabolic and reproductive plasticity.iScience · 2026Article
- Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms.Nature communications · 2026Article
- Novel INSL3 variants cause male infertility with cryptorchidism.Journal of assisted reproduction and genetics · 2026Article
- Tumor-secreted clusterin promotes cachectic fat wasting via disrupting circadian gene expression and adipogenesis.The EMBO journal · 2026Article
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Transcriptional regulation of neuropeptide receptors underlies context-dependent adaptation in Drosophila melanogaster.FEBS open bio · 2026Article
- Comprehensive insights into emerging advances in the Neurobiology of anorexia.Journal of advanced research · 2026Review
- SIFa peptidergic neurons orchestrate the internal states and energy balance of male Drosophila melanogaster.PLoS biology · 2025Article
- Adipose tissue-secreted Spz5 promotes distal tumor progression via Toll-6-mediated Hh pathway activation in Drosophila.The EMBO journal · 2025Article
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- Mechanisms and pharmacotherapy of cancer cachexia-associated anorexia.Pharmacology research & perspectives · 2025Review
- Insulin-like peptide 3 is not a biomarker for pancreatic ductal adenocarcinoma.Frontiers in endocrinology · 2025Article
- The Power of Drosophila in Modeling Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- Paraneoplastic renal dysfunction in fly cancer models driven by inflammatory activation of stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Discovery of RXFP2 genetic association in resistant hypertensive men and RXFP2 antagonists for the treatment of resistant hypertension.Scientific reports · 2024Article
- AZGP1 in POMC neurons modulates energy homeostasis and metabolism through leptin-mediated STAT3 phosphorylation.Nature communications · 2024Article
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12 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In patients with advanced-stage cancer, cancer-associated anorexia affects treatment success and patient survival. However, the underlying mechanism is poorly understood. Here, we show that Dilp8, a Drosophila homologue of mammalian insulin-like 3 peptide (INSL3), is secreted from tumour tissues and induces anorexia through the Lgr3 receptor in the brain. Activated Dilp8-Lgr3 signalling upregulated anorexigenic nucleobinding 1 (NUCB1) and downregulated orexigenic short neuropeptide F (sNPF) and NPF expression in the brain. In the cancer condition, the protein expression of Lgr3 and NUCB1 was significantly upregulated in neurons expressing sNPF and NPF. INSL3 levels were increased in tumour-implanted mice and INSL3-treated mouse hypothalamic cells showed Nucb2 upregulation and Npy downregulation. Food consumption was significantly reduced in intracerebrospinal INSL3-injected mice. In patients with pancreatic cancer, higher serum INSL3 levels increased anorexia. These results indicate that tumour-derived Dilp8/INSL3 induces cancer anorexia by regulating feeding hormones through the Lgr3/Lgr8 receptor in Drosophila and mammals.
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