ArticleJournal of molecular medicine (Berlin, Germany)2019
Dichotomal functions of phosphorylated and unphosphorylated STAT1 in hepatocellular carcinoma.
Article in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The trial behind it
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Post‑translational modifications in atherosclerosis: Roles, mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Evolving Landscape of Systemic Therapy for Hepatocellular Carcinoma: From Targeted Therapy and Combination Strategies to Emerging Therapies.Biomedicines · 2026Review
- CYP8B1 inhibits hepatocellular carcinoma progression by repressing PAK4 transcription through inhibition of nuclear translocation of u-STAT1.Cell death & disease · 2025Article
- Review
- Lestaurtinib Has the Potential to Inhibit the Proliferation of Hepatocellular Carcinoma Uncovered by Bioinformatics Analysis and Pharmacological Experiments.Frontiers in cell and developmental biology · 2022Article
- Inflammatory response of gut, spleen, and liver in mice induced by orally administeredJournal of oral microbiology · 2022Article
- Drug Discovery in Liver Disease Using Kinome Profiling.International journal of molecular sciences · 2021Review
- Article
- LpCat1 Promotes Malignant Transformation of Hepatocellular Carcinoma Cells by Directly Suppressing STAT1.Frontiers in oncology · 2021Article
- JAK/STAT signaling in hepatocellular carcinoma.Hepatic oncology · 2020Review
- Article
- Jak-Stat Signaling Induced by Interleukin-6 Family Cytokines in Hepatocellular Carcinoma.Cancers · 2019Review
- Machine-Learning-Based Identification of Key Feature RNA-Signature Linked to Diagnosis of Hepatocellular Carcinoma.Journal of clinical and experimental hepatologyArticle
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Interferons (IFNs) with antiviral and immune-stimulatory functions have been widely used in prevention and treatment of hepatocellular carcinoma (HCC). Signal transducer and activator of transcription 1 (STAT1) is a key element of the IFN signaling, and the function of STAT1 is critically determined by its phosphorylation state. This study aims to understand the functions of phosphorylated (p-) and unphosphorylated (u-) STAT1 in HCC. We found that u-STAT1 is significantly elevated in patient HCC tumor tissues and predominantly expressed in cytoplasm; while p-STAT1 is absent. Loss of u-STAT1 potently arrested cell cycle and inhibited cell growth in HCC cells. Induction of p-STAT1 by IFN-α treatment effectively triggers the expression of interferon-stimulated genes (ISGs), but has moderate effect on HCC cell growth. Interestingly, both u-STAT1 and p-STAT1 are induced by IFN-α, through with distinct time-dependent process. Furthermore, the ISG induction patterns mediated by p-STAT1 and u-STAT1 are also distinct. Importantly, artificial blocking of the induction of u-STAT1, but not p-STAT1, sensitizes HCC cells to treatment of IFNs. Therefore, p-STAT1 and u-STAT1 exert dichotomal functions and coordinately regulate the responsiveness to IFN treatment in HCC. KEY MESSAGES: STAT1 is upregulated and predominantly presented as u-STAT1 in HCC, while p-STAT1 is absent. U-STAT1 sustains but p-STAT1 inhibits HCC growth. The dynamic change of phosphorylation state of STAT1 control the responsiveness to IFN treatment.
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Registered trials
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