ArticleEMBO molecular medicine2013
TSC22D4 is a molecular output of hepatic wasting metabolism.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- A Randomized Phase II Study of Irinotecan Plus Cisplatin with or without Simvastatin in Ever-Smokers with Extended Disease Small Cell Lung Cancer.Cancer research and treatment · 2023Trial
- microRNA-379 couples glucocorticoid hormones to dysfunctional lipid homeostasis.The EMBO journal · 2015Trial
- TSC22D4 drives clear cell renal cell carcinoma progression and therapy resistance by stabilizing NRF2 through KEAP1 disruption.Cell death & disease · 2026Article
- The effects of tissue inflammation on cancer cachexia.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- Novel Insights into TSC22D Family Genes in Metabolic Diseases and Cancer.Biomolecules · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Comparative Transcriptomic Analysis Reveals Key Growth-Related Genes and Alternative Splicing Events in Siniperca scherzeri.Marine biotechnology (New York, N.Y.) · 2025Article
- Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024Review
- Leukemia inhibitory factor suppresses hepatic de novo lipogenesis and induces cachexia in mice.Nature communications · 2024Article
- Tricarboxylic acid (TCA) cycle, sphingolipid, and phosphatidylcholine metabolism are dysregulated inHeliyon · 2023Article
- Progressive development of melanoma-induced cachexia differentially impacts organ systems in mice.Cell reports · 2023Article
- TSC22D4 interacts with Akt1 to regulate glucose metabolism.Science advances · 2022Article
- Hepatocyte-specific activity of TSC22D4 triggers progressive NAFLD by impairing mitochondrial function.Molecular metabolism · 2022Article
- Pathological features of tissues and cell populations during cancer cachexia.Cell regeneration (London, England) · 2022Review
- Cancer cachexia as a multiorgan failure: Reconstruction of the crime scene.Frontiers in cell and developmental biology · 2022Review
- [Parathyroid hormone-related protein aggravates nonalcoholic fatty liver disease induced by methionine choline-deficient diet in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- A novel tissue inhibitor of metalloproteinases-1/liver/cachexia score predicts prognosis of gastrointestinal cancer patients.Journal of cachexia, sarcopenia and muscle · 2021Article
- Multi-compartment metabolomics and metagenomics reveal major hepatic and intestinal disturbances in cancer cachectic mice.Journal of cachexia, sarcopenia and muscle · 2021Article
- Inflammation-induced cholestasis in cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2021Article
- Glucose Metabolism Reprogramming of Primary Tumor and the Liver Is Associated With Disease-Free Survival in Patients With Early NSCLC.Frontiers in oncology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, proper storage and distribution of lipids in and between tissues is essential for the maintenance of energy homeostasis. Here, we show that tumour growth triggers hepatic metabolic dysfunction as part of the cancer cachectic phenotype, particularly by reduced hepatic very-low-density-lipoprotein (VLDL) secretion and hypobetalipoproteinemia. As a molecular cachexia output pathway, hepatic levels of the transcription factor transforming growth factor beta 1-stimulated clone (TSC) 22 D4 were increased in cancer cachexia. Mimicking high cachectic levels of TSC22D4 in healthy livers led to the inhibition of hepatic VLDL release and lipogenic genes, and diminished systemic VLDL levels under both normal and high fat dietary conditions. Liver-specific ablation of TSC22D4 triggered hypertriglyceridemia through the induction of hepatic VLDL secretion. Furthermore, hepatic TSC22D4 expression levels were correlated with the degree of body weight loss and VLDL hypo-secretion in cancer cachexia, and TSC22D4 deficiency rescued tumour cell-induced metabolic dysfunction in hepatocytes. Therefore, hepatic TSC22D4 activity may represent a molecular rationale for peripheral energy deprivation in subjects with metabolic wasting diseases, including cancer cachexia.
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