Observational studyCellular and molecular gastroenterology and hepatology2020
Forkhead Box M1 Transcription Factor Drives Liver Inflammation Linking to Hepatocarcinogenesis in Mice.
Observational study in Cellular and molecular gastroenterology and hepatology, 2020. 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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17 citing papers in PubMed, 28 citations in OpenAlex.
- A peptide-based PROTAC targeting FOXM1 suppresses fibrosis-associated hepatocarcinogenesis.Theranostics · 2026Article
- The oncogenic role of FOXM1 in hepatocellular carcinoma: molecular mechanisms, clinical significance, and therapeutic potentials.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Research progress of CD73-adenosine signaling regulating hepatocellular carcinoma through tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2025Review
- Hormone correction of dysfunctional metabolic gene expression in stem cell-derived liver tissue.Stem cell research & therapy · 2025Article
- Role of the FOXM1/CMA/ER stress axis in regulating the progression of nonalcoholic steatohepatitis.Clinical and translational medicine · 2025Article
- Interaction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development.Cell division · 2025Article
- The conformation of FOXM1 homodimers in vivo is crucial for regulating transcriptional activities.Nucleic acids research · 2024Article
- The role of forkhead box M1-methionine adenosyltransferase 2 A/2B axis in liver inflammation and fibrosis.Nature communications · 2024Article
- Review
- Transcription factor FoxM1 promotes cyst growth in PKD1 mutant ADPKD.Human molecular genetics · 2023Article
- Regulatory mechanism of downregulation of SOD1 expression on cardiomyocyte function.Sleep & breathing = Schlaf & Atmung · 2023Article
- Forkhead Domain Inhibitor-6 Suppresses Corneal Neovascularization and Subsequent Fibrosis After Alkali Burn in Rats.Investigative ophthalmology & visual science · 2022Article
- HELLS Is Negatively Regulated by Wild-Type P53 in Liver Cancer by a Mechanism Involving P21 and FOXM1.Cancers · 2022Article
- Distinct roles of KLF4 in mesenchymal cell subtypes during lung fibrogenesis.Nature communications · 2021Article
- Analysis of Bulk RNA Sequencing Data Reveals Novel Transcription Factors Associated With Immune Infiltration Among Multiple Cancers.Frontiers in immunology · 2021Article
- Liver Fibrosis and Inflammation under the Control of ERK2.International journal of molecular sciences · 2020Article
- FoxM1 Induces CCl2 Secretion From Hepatocytes Triggering Hepatic Inflammation, Injury, Fibrosis, and Liver Cancer.Cellular and molecular gastroenterology and hepatology · 2020Article
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Authors and funding
18 authors at 2 institutions in 3 countries.
Funding
Abstract
BACKGROUND &
aimsLiver inflammation has been recognized as a hallmark of hepatocarcinogenesis. Although Forkhead Box M1 (FoxM1) is a well-defined oncogenic transcription factor that is overexpressed in hepatocellular carcinoma (HCC), its role in liver inflammation has never been explored.
methodsWe generated hepatocyte-specific FoxM1 conditional transgenic (TG) mice by using the Cre-loxP and Tetracycline (Tet)-on systems to induce FoxM1 expression in a hepatocyte-specific and time-dependent manner.
resultsAfter treatment of Tet-derivatives doxycycline (DOX) to induce FoxM1, TG mice exhibited spontaneous development of hepatocyte death with elevated serum alanine aminotransferase levels and hepatic infiltration of macrophages. The removal of DOX in TG mice completely removed this effect, suggesting that spontaneous inflammation in TG mice occurs in a hepatocyte FoxM1-dependent manner. In addition, liver inflammation in TG mice was associated with increased levels of hepatic and serum chemokine (C-C motif) ligand 2 (CCL2). In vitro transcriptional analysis confirmed that CCL2 is a direct target of FoxM1 in murine hepatocytes. After receiving FoxM1 induction since birth, all TG mice exhibited spontaneous HCC with liver fibrosis at 12 months of age. Hepatic expression of FoxM1 was significantly increased in liver injury models. Finally, pharmacologic inhibition of FoxM1 reduced liver inflammation in models of liver injury.
conclusionsHepatocyte FoxM1 acts as a crucial regulator to orchestrate liver inflammation linking to hepatocarcinogenesis. Thus, hepatocyte FoxM1 may be a potential target not only for the treatment of liver injury but also for the prevention toward HCC.
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