ArticleNature communications2024
Area postrema neurons mediate interleukin-6 function in cancer cachexia.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Neural-tumor interactions: bidirectional regulatory mechanisms and nervous system-targeted tumor therapeutic strategies.Biomarker research · 2026Review
- The causes of cachexia: key signals and the brain.Nature reviews. Endocrinology · 2026Review
- Decoding neuro-tumor interactions in pancreatic cancer: mechanisms, immunosuppressive networks and therapeutic opportunities.Molecular biomedicine · 2026Review
- Cancer Neuroscience: From Local Neuro-Immune Microenvironments to Systemic Brain-Body Circuitry.MedComm · 2026Review
- Neural regulation of cancer: from microenvironmental hijacking to systemic circuit co-option.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Feeding Behaviour in the KPC Model of Pancreatic Cancer-Associated Cachexia: Alteration of Spontaneous and Evoked Feeding Behaviours.Journal of cachexia, sarcopenia and muscle · 2026Article
- Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms.Nature communications · 2026Article
- Aberrant hypothalamic neuronal activity blunts glucocorticoid diurnal rhythms in murine breast cancer.Neuron · 2026Article
- Lipids grease the chain of cancer progression.Trends in cancer · 2026Review
- Fos-induced osteosarcoma growth causes a cachexia-like phenotype in mice and correlates with high Fgf21 serum levels.Cancer & metabolism · 2026Article
- Mechanistic insights into the liver-brain axis during chronic liver disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- Brain Nutrient Sensing: A Unifying Framework.Annual review of physiology · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Exercise-modulated IL-6 in cancer cachexia: molecular mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- Exercise as a multiscale recalibration of stress-related homeostatic balance.Frontiers in neuroscience · 2026Review
- Bidirectional crosstalk between the nervous system and the tumour microenvironment: mechanisms, feedback loops and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Interleukin-6, anxiety, and pre-treatment malnutrition in locally advanced head and neck cancer: a psychoneuroimmunological analysis.Frontiers in nutrition · 2026Article
- Region-Specific Adult Neural Stem Cell Niches of the Mediobasal Hypothalamus and Medulla Oblongata.Stem cell reviews and reports · 2026Review
- Critical changes in whole-brain gene networks in response to small-cell lung cancer as revealed by single-nucleus RNA sequencing.Frontiers in immunology · 2026Article
- Brain-immune interactions generate pathogen-specific sickness states.bioRxiv : the preprint server for biology · 2025Article
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10 authors.
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Abstract
Interleukin-6 (IL-6) has been long considered a key player in cancer cachexia. It is believed that sustained elevation of IL-6 production during cancer progression causes brain dysfunctions, which ultimately result in cachexia. However, how peripheral IL-6 influences the brain remains poorly understood. Here we show that neurons in the area postrema (AP), a circumventricular structure in the hindbrain, is a critical mediator of IL-6 function in cancer cachexia in male mice. We find that circulating IL-6 can rapidly enter the AP and activate neurons in the AP and its associated network. Peripheral tumor, known to increase circulating IL-6, leads to elevated IL-6 in the AP, and causes potentiated excitatory synaptic transmission onto AP neurons and AP network hyperactivity. Remarkably, neutralization of IL-6 in the brain of tumor-bearing mice with an anti-IL-6 antibody attenuates cachexia and the hyperactivity in the AP network, and markedly prolongs lifespan. Furthermore, suppression of Il6ra, the gene encoding IL-6 receptor, specifically in AP neurons with CRISPR/dCas9 interference achieves similar effects. Silencing Gfral-expressing AP neurons also attenuates cancer cachectic phenotypes and AP network hyperactivity. Our study identifies a central mechanism underlying the function of peripheral IL-6, which may serve as a target for treating cancer cachexia.
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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.