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Updated: Mar 27, 2026
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Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
Published on: July 18, 2025
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From steatosis to metastasis: microenvironmental reprogramming of the liver in metabolic dysfunction-associated
Gyu Jeong Cho1, Sun Myoung Kim1, Yoon Mee Yang2
1School of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Clinical and Molecular Hepatology
|March 25, 2026
Summary
Metabolic dysfunction-associated steatotic liver disease (MASLD) creates a pro-metastatic liver environment. Targeting specific pathways in MASLD may restore antitumor immunity and improve colorectal cancer liver metastasis treatment.
Area of Science:
- Hepatology and oncology
- Cancer metastasis research
Background:
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a risk factor for primary and extrahepatic cancers.
- MASLD promotes a liver microenvironment conducive to tumor growth and metastasis, particularly for colorectal cancer.
- Tumor-stromal interactions within the steatotic liver are critical drivers of colorectal cancer liver metastasis.
Purpose of the Study:
- To review the mechanisms by which MASLD facilitates colorectal cancer liver metastasis.
- To summarize key pathways contributing to a pre- and pro-metastatic niche in the liver.
- To discuss potential therapeutic strategies targeting these pathways to restore antitumor immunity.
Main Methods:
- Literature review of studies investigating MASLD and colorectal cancer liver metastasis.
- Analysis of molecular and cellular mechanisms driving tumor-stromal interactions in the liver.
- Evaluation of therapeutic targets for improving antitumor immunity and treatment response.
Main Results:
- MASLD supports liver metastasis through mechanisms including extracellular vesicles, hyaluronic acid production, M2 macrophage infiltration, and YAP signaling.
- Key pathways identified include EV-mediated communication, tumor-stromal feedback loops, and HA-induced ECM remodeling.
- These processes impair antitumor immunity and promote immune escape in the liver microenvironment.
Conclusions:
- MASLD establishes a pro-metastatic niche in the liver that hinders anti-tumor immunity.
- Targeting hyaluronic acid synthesis, IL-1 signaling, or CXCR2 may restore immunity.
- These strategies show promise for enhancing responses to PD-1 blockade in colorectal cancer liver metastasis.
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