Related Experiment Video
Updated: Jan 19, 2026
A "Patient-Like" Orthotopic Syngeneic Mouse Model of Hepatocellular Carcinoma Metastasis
Published on: October 24, 2015
Dimethyl fumarate suppresses hepatocellular carcinoma progression via activating SOCS3/JAK1/STAT3 signaling pathway
Hua Liu1,2, Xiao-De Feng1,2, Beng Yang1,3
1Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital, School of Medicine, Zhejiang University Zhejiang Province, China.
Abstract:
Dimethyl fumarate (DMF) is generally used to treat psoriasis and multiple sclerosis. In the present study, we aimed to investigate the effects of DMF on hepatocellular carcinoma progression and its mechanism of action. In vitro, cell viability was examined using CCK-8 assay; cell cycle was analyzed by flow cytometry; angiogenesis was detected using tube formation assay; and autophagic flux assay results were examined using fluorescence microscopy. We also used western blotting to explore the potential mechanisms. In vivo, tumor xenograft experiment was performed with nude mice, and liver function, renal function, and routine blood counts were assessed using biochemical tests. Dimethyl fumarate inhibited tumor growth and angiogenesis in hepatocellular carcinoma, both in vitro and in vivo. Dimethyl fumarate decreased autophagy in hepatocellular carcinoma cells. Treatment with DMF activated SOCS3, which led to repression of JAK1 and STAT3 phosphorylation. DMF inhibited cell proliferation, angiogenesis, and autophagy via activation of the SOCS3/JAK1/STAT3 signaling pathway. This finding may provide a novel approach for the treatment of hepatocellular carcinoma.
Insights
Dimethyl fumarate (DMF) effectively inhibits hepatocellular carcinoma growth and angiogenesis by decreasing autophagy. DMF activates the SOCS3/JAK1/STAT3 pathway, offering a potential new treatment strategy for liver cancer.
Area of Science:
- Oncology
- Pharmacology
Background:
- Dimethyl fumarate (DMF) is an established treatment for psoriasis and multiple sclerosis.
- Hepatocellular carcinoma (HCC) remains a significant global health challenge with limited therapeutic options.
Purpose of the Study:
- To investigate the anti-cancer effects of Dimethyl fumarate (DMF) on hepatocellular carcinoma (HCC) progression.
- To elucidate the underlying molecular mechanisms of DMF action in HCC.
Main Methods:
- In vitro studies included CCK-8 assays, flow cytometry for cell cycle analysis, tube formation assays for angiogenesis, and fluorescence microscopy for autophagic flux.
- Western blotting was employed to analyze protein expression and signaling pathways.
- In vivo studies involved tumor xenograft models in nude mice, with assessments of liver function, renal function, and blood counts.
Main Results:
- Dimethyl fumarate demonstrated significant inhibition of tumor growth and angiogenesis in HCC models, both in vitro and in vivo.
- DMF treatment led to decreased autophagy in HCC cells.
- DMF activated Suppressor of Cytokine Signaling 3 (SOCS3), subsequently repressing Janus Kinase 1 (JAK1) and Signal Transducer and Activator of Transcription 3 (STAT3) phosphorylation.
Conclusions:
- Dimethyl fumarate inhibits HCC cell proliferation, angiogenesis, and autophagy through the activation of the SOCS3/JAK1/STAT3 signaling pathway.
- These findings suggest DMF as a potential novel therapeutic agent for hepatocellular carcinoma.
Related Concept Videos
05:06A "Patient-Like" Orthotopic Syngeneic Mouse Model of Hepatocellular Carcinoma Metastasis
13:38Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
05:31Transradial Access Chemoembolization for Hepatocellular Carcinoma Patients
10:35Generation of Subcutaneous and Intrahepatic Human Hepatocellular Carcinoma Xenografts in Immunodeficient Mice
08:25Mass Cytometry Analysis of Systemic and Local Immune Responses in Hepatocellular Carcinoma
07:47Non-Invasive PET/MR Imaging in an Orthotopic Mouse Model of Hepatocellular Carcinoma