ArticleSignal transduction and targeted therapy2026
Metabolic dysfunction-associated steatotic liver disease accelerates pancreatic cancer progression and metastasis via the macrophage migration inhibitory factor-CD44 axis.
Article in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Effect of reduction in skeletal muscle quantity and sex differences on postoperative hepatic steatosis following total pancreatectomy.Surgery today · 2026Article
- MASLD and Pancreatic Diseases: From Shared Mechanisms to Clinical Implications and Future Directions.Nutrients · 2026Review
- MIF-Associated Immunosuppressive CAF Remodeling Predicts Poor Prognosis During Lung Adenocarcinoma Progression: A Single-Cell and Multicohort Transcriptomic Study.Biomedicines · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and immune checkpoint inhibitor response in gastrointestinal liver metastases: current evidence and future directions.Frontiers in nutrition · 2026Review
- M1 macrophage-targeted engineered ginseng stems and leaves-derived extracellular vesicles delivery system for alleviating rheumatoid arthritis.Regenerative biomaterials · 2026Article
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Authors and funding
41 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a poor prognosis, particularly in the presence of liver metastases. The mechanisms by which metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), influences PDAC progression and metastasis remain poorly understood. This study investigates the role of MASLD in fostering an immunosuppressive microenvironment conducive to PDAC liver metastases and identifies the macrophage migration inhibitory factor (MIF)-CD44 axis as a key mediator of this process. Utilizing data from the UK Biobank (450,754 participants, median follow-up 14.5 years), we observed an overall increased risk of PDAC in the MASLD population (HR: 3.48; 95% CI: 2.69-4.50; P < 0.0001). Clinical cohorts confirmed the strong association between MASLD and hepatic metastases (OR: 7.06; 95% CI: 4.62-10.78; P < 0.0001). Experimental mouse models demonstrated that MASLD enhances tumor cell stemness, immune evasion, and focal adhesion in metastatic liver tissues. Mechanistically, MASLD-induced MIF secretion promotes CD44-positive PDAC cell migration, stemness, and adhesion. Targeting MIF, either genetically or pharmacologically using the MIF tautomerase inhibitor IPG1576 significantly attenuated liver metastasis in preclinical models. Validation in patient samples revealed elevated hepatic MIF and CD44 expression in MASLD-associated PDAC liver metastases. This study highlights the MIF-CD44 axis as a promising therapeutic target and underscores the importance of tailoring treatments for PDAC patients with concurrent MASLD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.