ArticleFrontiers in oncology2022
Cytokine-Mediated STAT3 Transcription Supports ATGL/CGI-58-Dependent Adipocyte Lipolysis in Cancer Cachexia.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting host ferroptosis in cancer cachexia: Tumor-immune triggers, tissue wasting, and the therapeutic paradox.iScience · 2026Review
- Inflammatory and catabolic activity mediate the association of plasma β-hydroxybutyrate and mortality in heart failure.ESC heart failure · 2026Observational
- Cancer-associated adipocytes: metabolic reprogramming, crosstalk and therapeutic implications in tumor progression.Signal transduction and targeted therapy · 2026Review
- STAT Signaling in Metabolic Disorders: From Molecular Mechanisms to Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Pro-inflammatory cytokine-driven molecular signaling in skeletal muscle during cancer cachexia.Biochemical Society transactions · 2026Review
- Lipids grease the chain of cancer progression.Trends in cancer · 2026Review
- Current Research Progress on ABHD5 in Cancers.Cancers · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Mechanosensitive Ion Channels: Molecular Hubs Integrating Skeletal Muscle Adaptation and Systemic Homeostasis.International journal of biological sciences · 2026Review
- Associations of systemic immune-inflammation index, product of platelet, and neutrophil count, with the pathological grade of bladder cancer.The Canadian journal of urology · 2025Article
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- The LEAP2 Response to Cancer-Related Anorexia-Cachexia Syndrome in Male Mice and Patients.Endocrinology · 2024Article
- Application of PPAR Ligands and Nanoparticle Technology in Metabolic Steatohepatitis Treatment.Biomedicines · 2024Review
- Testosterone Inhibits Lipid Accumulation in Porcine Preadipocytes by RegulatingAnimals : an open access journal from MDPI · 2024Article
- Leukemia inhibitory factor suppresses hepatic de novo lipogenesis and induces cachexia in mice.Nature communications · 2024Article
- STAT3 Signalling Drives LDH Up-Regulation and Adiponectin Down-Regulation in Cachectic Adipocytes.International journal of molecular sciences · 2023Article
- Melanoma cells induce dedifferentiation and metabolic changes in adipocytes present in the tumor niche.Cellular & molecular biology letters · 2023Article
- Systemic Reprogramming of Endothelial Cell Signaling in Metastasis and Cachexia.Physiology (Bethesda, Md.) · 2023Review
- Mutual impact of adipocytes and colorectal cancer cells growing in co-culture conditions.Cell communication and signaling : CCS · 2023Article
- Tumor loss-of-function mutations in STK11/LKB1 induce cachexia.JCI insight · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Adipose tissue inflammation is observed in multiple metabolically-altered states including cancer-associated cachexia and obesity. Although cachexia is a syndrome of adipose loss and obesity is a disease of adipose excess, both pathologies demonstrate increases in circulating levels of IL-6 family cytokines, β-adrenergic signaling, and adipocyte lipolysis. While β-adrenergic-stimulated adipocyte lipolysis is well described, there is limited mechanistic insight into how cancer cachexia-associated inflammatory cytokines contribute to adipocyte lipolysis under pathologic conditions. Here, we set out to compare adipocyte lipolysis signaling by cancer cachexia-associated IL-6 family cytokines (IL-6 and LIF) to that of the β-adrenergic agonist isoproterenol. Unlike isoproterenol, the IL-6 family of cytokines required JAK/STAT3-dependent transcriptional changes to induce adipocyte lipolysis. Furthermore, cachexia-associated cytokines that used STAT3 to induce lipolysis were primarily dependent on the lipase ATGL and its cofactor CGI-58 rather than lipases HSL and MAGL. Finally, administration of JAK but not β-adrenergic inhibitors suppressed adipose STAT3 phosphorylation and associated adipose wasting in a murine model of cancer cachexia characterized by increased systemic IL-6 family cytokine levels. Combined, our results demonstrate how the IL-6 family of cytokines diverge from β-adrenergic signals by employing JAK/STAT3-driven transcriptional changes to promote adipocyte ATGL/CGI-58-dependent lipolysis contributing to adipose wasting in cancer cachexia.
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