ArticleNature communications2022
Hepatocyte phosphatase DUSP22 mitigates NASH-HCC progression by targeting FAK.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
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- Analysis and validation of abnormal signaling pathways and immune cell infiltration characteristics in digestive system cancers based on peroxisome-related genes.Biology direct · 2026Article
- Gene therapy for liver diseases: methods, challenges and opportunities.Journal of nanobiotechnology · 2026Review
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
- The dual-specificity phosphatase JSP1 regulates neutrophil adhesion via integrin-SRC signaling in vascular inflammation.The Journal of biological chemistry · 2026Article
- OCTN2 Activates a Non-Canonical Carnitine Metabolic Pathway to Promote MASH-HCC Progression and Immunotherapy Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dysfunctional TRIM31 of POMC Neurons Provokes Hypothalamic Injury and Peripheral Metabolic Disorder under Long-Term Fine Particulate Matter Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hepatocyte TonEBP promotes metabolic stress-induced hepatic fibroinflammation involving transcriptional activation of ELR⁺ CXC chemokines.Cell death discovery · 2026Article
- Quantification of overall tumor burden using longitudinal magnetic resonance imaging improves response assessment in orthotopic murine hepatocellular carcinoma models.Scientific reports · 2026Article
- DUSP22 dephosphorylates LGALS1 to enhance T cell-driven antitumor immunity.Journal for immunotherapy of cancer · 2026Article
- RhoE downregulation leads to enhanced cholesterol biosynthesis and sorafenib resistance in hepatocellular carcinoma.The Journal of biological chemistry · 2025Article
- Ultra-small coordination dihydromyricetin nanodots attenuate alveolar bone resorption in periodontitis through inhibition of ITGB3-Driven osteoclast differentiation.Materials today. Bio · 2025Article
- Mesenchymal stem cells improve ovarian function by suppressing fibrosis through CTGF/FAK signalling in systemic lupus erythematosus.Lupus science & medicine · 2025Article
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- Mapping administration route-dependent transduction profiles of commonly used AAV variants in mice by barcode amplicon sequencing.Molecular therapy. Methods & clinical development · 2025Article
- Review
- Focal adhesion kinase promotes aerobic glycolysis in hepatic stellate cells via the cyclin D1/c-Myc/MCT-1 pathway to induce liver fibrosis.Scientific reports · 2025Article
- Luteolin-7-diglucuronide, a novel PTP1B inhibitor, ameliorates hepatic stellate cell activation and liver fibrosis in mice.Acta pharmacologica Sinica · 2025Article
- Serum JKAP as a potential prognostic biomarker in acute coronary syndrome patients undergoing percutaneous coronary intervention.Frontiers in cardiovascular medicine · 2025Article
- Piezo1 Regulates Stiffness-Dependent DRG Axon Regeneration via Modifying Cytoskeletal Dynamics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic steatohepatitis (NASH), a common clinical disease, is becoming a leading cause of hepatocellular carcinoma (HCC). Dual specificity phosphatase 22 (DUSP22, also known as JKAP or JSP-1) expressed in numerous tissues plays essential biological functions in immune responses and tumor growth. However, the effects of DUSP22 on NASH still remain unknown. Here, we find a significant decrease of DUSP22 expression in human and murine fatty liver, which is mediated by reactive oxygen species (ROS) generation. Hepatic-specific DUSP22 deletion particularly exacerbates lipid deposition, inflammatory response and fibrosis in liver, facilitating NASH and non-alcoholic fatty liver disease (NAFLD)-associated HCC progression. In contrast, transgenic over-expression, lentivirus or adeno-associated virus (AAV)-mediated DUSP22 gene therapy substantially inhibit NASH-related phenotypes and HCC development in mice. We provide mechanistic evidence that DUSP22 directly interacts with focal adhesion kinase (FAK) and restrains its phosphorylation at Tyr397 (Y397) and Y576 + Y577 residues, subsequently prohibiting downstream activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor-κB (NF-κB) cascades. The binding of DUSP22 to FAK and the dephosphorylation of FAK are indispensable for DUSP22-meliorated NASH progression. Collectively, our findings identify DUSP22 as a key suppressor of NASH-HCC, and underscore the DUSP22-FAK axis as a promising therapeutic target for treatment of the disease.
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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 Socratic graph.