ArticleCancer cell2010
TAK1 suppresses a NEMO-dependent but NF-kappaB-independent pathway to liver cancer.
Article in Cancer cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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Who cites it
128 citing papers in PubMed, 219 citations in OpenAlex.
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- Dual signaling pathways of TGF-β superfamily cytokines in hepatocytes: balancing liver homeostasis and disease progression.Frontiers in pharmacology · 2025Review
- Clinical and preclinical studies of mesenchymal stem cells to alleviate peritoneal fibrosis.Stem cell research & therapy · 2024Review
- Implications of neonatal absence of innate immune mediated NFκB/AP1 signaling in the murine liver.Pediatric research · 2024Article
- Disruption of TIGAR-TAK1 alleviates immunopathology in a murine model of sepsis.Nature communications · 2024Article
- The role of novel adipokines in hepatocellular carcinoma progression: a mini review.American journal of cancer research · 2024Review
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- CAFs-derived SCUBE1 promotes malignancy and stemness through the Shh/Gli1 pathway in hepatocellular carcinoma.Journal of translational medicine · 2022Article
- Imbalanced gut microbiota fuels hepatocellular carcinoma development by shaping the hepatic inflammatory microenvironment.Nature communications · 2022Article
- Nuclear HMGB1 protects from nonalcoholic fatty liver disease through negative regulation of liver X receptor.Science advances · 2022Article
- Clinical significance of mitogen-activated protein kinase kinase kinases in hepatitis B virus -related hepatocellular carcinoma and underlying mechanism exploration.Bioengineered · 2022Article
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- Prognostic signature composed of transcription factors accurately predicts the prognosis of gastric cancer patients.Cancer cell international · 2021Article
- Review
68 more citing papers are in PubMed but not listed here.
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Authors and funding
27 authors at 8 institutions in 6 countries.
Funding
Abstract
The MAP3-kinase TGF-beta-activated kinase 1 (TAK1) critically modulates innate and adaptive immune responses and connects cytokine stimulation with activation of inflammatory signaling pathways. Here, we report that conditional ablation of TAK1 in liver parenchymal cells (hepatocytes and cholangiocytes) causes hepatocyte dysplasia and early-onset hepatocarcinogenesis, coinciding with biliary ductopenia and cholestasis. TAK1-mediated cancer suppression is exerted through activating NF-kappaB in response to tumor necrosis factor (TNF) and through preventing Caspase-3-dependent hepatocyte and cholangiocyte apoptosis. Moreover, TAK1 suppresses a procarcinogenic and pronecrotic pathway, which depends on NF-kappaB-independent functions of the I kappaB-kinase (IKK)-subunit NF-kappaB essential modulator (NEMO). Therefore, TAK1 serves as a gatekeeper for a protumorigenic, NF-kappaB-independent function of NEMO in parenchymal liver cells.
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Registered trials
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.