ArticleOncoimmunology2021
NFATc3 inhibits hepatocarcinogenesis and HBV replication via positively regulating RIG-I-mediated interferon transcription.
Article in Oncoimmunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- HBV reprograms the tumor microenvironment in hepatocellular carcinoma: mechanisms and therapeutic implications.Clinical and experimental medicine · 2026Review
- NFATC3 enhances osteosarcoma progression by increasing PD-L1 and CXCL2 levels.Medical oncology (Northwood, London, England) · 2025Article
- Pan-cancer analysis of UDP-glucose 6-dehydrogenase in human tumors and its function in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- Synthetic RIG-I-Agonist RNA Induces Death of Hepatocellular Carcinoma Cells.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025Article
- Identification of cis-sQTL demonstrates genetic associations and functional implications of inflammatory processes in Nelore cattle muscle tissue.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Antiviral Therapy-Induced Changes in Long Non-Coding RNA Expression Profiles in Umbilical Cord Blood and Placental Tissues of Hepatitis B Virus-Infected Pregnant Women.International journal of women's health · 2025Article
- Nuclear Factor of Activated T Cells (NFAT) Proteins as Targeted Molecules in Diseases: A Narrative Review.Cureus · 2024Review
- Mechanism of action and treatment of type I interferon in hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- RNA mFrontiers in immunology · 2024Review
- Transcriptome wide functional analysis of HBx expressing human hepatocytes stimulated with endothelial cell cross-talk.Genomics · 2023Article
- Identification and validation of cuproptosis related genes and signature markers in bronchopulmonary dysplasia disease using bioinformatics analysis and machine learning.BMC medical informatics and decision making · 2023Article
- Exploring the mechanism of JiGuCao capsule formula on treating hepatitis B virus infection via network pharmacology analysis andFrontiers in pharmacology · 2023Article
- Friend or foe: RIG- I like receptors and diseases.Autoimmunity reviews · 2022Review
- RIG-I Promotes Cell Viability, Colony Formation, and Glucose Metabolism and Inhibits Cell Apoptosis in Colorectal Cancer by NF-Disease markers · 2022Article
- Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection.Frontiers in cellular and infection microbiology · 2022Review
- NFAT as a Biomarker and Therapeutic Target in Non-Small Cell Lung Cancer-Related Brain Metastasis.Frontiers in oncology · 2021Article
- FGF19/SOCE/NFATc2 signaling circuit facilitates the self-renewal of liver cancer stem cells.Theranostics · 2021Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor of activated T cells 3 (NFATc3) has been reported to upregulate type I interferons (IFNs) expression, and the abnormal expression and activation of NFATc3 were closely related to tumorigenesis. However, the potential function of NFATc3 in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) remains to be elucidated. In this study, we found that NFATc3 gene was frequently deleted and downregulated in HCC tumor tissues, and that the downregulation of NFATc3 was associated with poor prognosis of HCC patients. The gain- and loss-of-function experiments demonstrated that NFATc3 inhibited HCC cell proliferation and invasion, as well as HBV replication. Mechanistically, NFATc3 could bind to the promoters of IFNL1 and IFNB1 genes and prompt the production of IFNs and interferon-stimulated genes. Furthermore, retinoic acid-inducible gene-I (RIG-I) pathway activation increased NFATc3 expression and nuclear localization, and activated NFATc3 further enhanced RIG-I-mediated IFN responses. Collectively, our findings reveal a novel regulatory signaling cascade, the RIG-I/NFATc3/IFNs axis, which inhibits hepatocarcinogenesis and HBV replication by enhancing the immune response in hepatocytes, and this functional axis might potentially be exploited for therapeutic benefits in the clinical treatment of HBV-related HCC.
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