Matrix viscoelasticity promotes liver cancer progression in the pre-cirrhotic liver
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Abstract
Type 2 diabetes mellitus is a major risk factor for hepatocellular carcinoma (HCC). Changes in extracellular matrix (ECM) mechanics contribute to cancer development 1,2 , and increased stiffness is known to promote HCC progression in cirrhotic conditions 3,4 . Type 2 diabetes mellitus is characterized by an accumulation of advanced glycation end-products (AGEs) in the ECM; however, how this affects HCC in non-cirrhotic conditions is unclear. Here we find that, in patients and animal models, AGEs promote changes in collagen architecture and enhance ECM viscoelasticity, with greater viscous dissipation and faster stress relaxation, but not changes in stiffness. High AGEs and viscoelasticity combined with oncogenic β-catenin signalling promote HCC induction, whereas inhibiting AGE production, reconstituting the AGE clearance receptor AGER1 or breaking AGE-mediated collagen cross-links reduces viscoelasticity and HCC growth. Matrix analysis and computational modelling demonstrate that lower interconnectivity of AGE-bundled collagen matrix, marked by shorter fibre length and greater heterogeneity, enhances viscoelasticity. Mechanistically, animal studies and 3D cell cultures show that enhanced viscoelasticity promotes HCC cell proliferation and invasion through an integrin-β1–tensin-1–YAP mechanotransductive pathway. These results reveal that AGE-mediated structural changes enhance ECM viscoelasticity, and that viscoelasticity can promote cancer progression in vivo, independent of stiffness.
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Accumulating evidence highlights ECM remodeling and tissue mechanics as active determinants of hepatocyte behavior.
“accumulating evidence highlights extracellular matrix (ECM) remodeling and tissue mechanics as active determinants of hepatocyte behavior [12, 13, 14, 15, 16].”
From Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction (2026) · cites this paper as [15]
The Abstract and “Matrix viscoelasticity activates YAP through TNS1” section show that ECM remodeling changes liver matrix mechanics and that increased viscoelasticity promotes HCC-cell proliferation and invasion. The claim extends this finding to hepatocyte behavior generally, whereas the reported cell-behavior experiments concern cancer cells. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThis mechanical alteration promotes hepatocellular carcinoma through the integrin-β1/tensin-1/YAP signaling pathway.
“This mechanical alteration promotes hepatocellular carcinoma through the integrin‐β1/tensin‐1/YAP signaling pathway.”
From Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction (2026) · cites this paper as [15]
In pre-cirrhotic NASH with type 2 diabetes, AGE-driven collagen remodeling increases ECM viscoelasticity without altering stiffness.
“in pre‐cirrhotic NASH with type 2 diabetes, advanced glycation product (AGE)‐driven collagen remodeling increases ECM viscoelasticity without altering stiffness.”
From Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction (2026) · cites this paper as [15]
Inhibition of AGE formation mitigates these effects.
“Inhibition of AGE formation mitigates these effects [15].”
From Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction (2026) · cites this paper as [15]
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- Authors
- Fan, W., Adebowale, K., Váncza, L., Li, Y., Rabbi, M. F., Kunimoto, K., Chen, D., Mozes, G., Chiu, D. K.-C., Li, Y., Tao, J., Wei, Y., Adeniji, N., Brunsing, R. L., Dhanasekaran, R., Singhi, A., Geller, D., Lo, S. H., Hodgson, L., Engleman, E. G., Charville, G. W., Charu, V., Monga, S. P., Kim, T., Wells, R. G., Chaudhuri, O., & Török, N. J.
- Affiliations
- VA Palo Alto Health Care System (US)
- Stanford University (US)
- Purdue University West Lafayette (US)
- Stanford Medicine (US)
- University of Pittsburgh (US)
- University of California, Davis (US)
- Albert Einstein College of Medicine (US)
- Keio University (JP)
- University of Pennsylvania (US)
- ORCID
- Fan, Weiguo
- Adebowale, Kolade
- Váncza, Lóránd
- Li, Yuan
- Rabbi, Md Foysal
- Mozes, Gergely
- Chiu, David Kung-Chun
- Li, Yisi
- Tao, Junyan
- Wei, Yi
- Adeniji, Nia
- Brunsing, Ryan L.
- Dhanasekaran, Renumathy
- Singhi, Aatur
- Geller, David
- Lo, Su Hao
- Hodgson, Louis
- Engleman, Edgar G.
- Charville, Gregory W.
- Charu, Vivek
- Monga, Satdarshan P.
- Kim, Taeyoon
- Wells, Rebecca G.
- Chaudhuri, Ovijit
- Török, Natalie J.
- Venue
- Nature
- Published
- 2024-01-31
- Volume
- 626
- Issue
- 7999
- Pages
- 635-642
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC10866704
- OpenAlex
- W4391383681
- Cited by
- 263
- References
- 61
- Citations by year
- 2026: 96 · 2025: 117 · 2024: 49 · 2023: 1
- FWCI
- 58.91
- Type
- journal article
- Language
- en
- Update notices
- correction (2025-11-27)
- Open access
- hybrid
- doi.org
- Locations
- Nature (publishedVersion, cc-by)
- Research Square (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Science Foundation (2026822)
- U.S. Department of Veterans Affairs (I01 BX002418)
- Stanford Diabetes Research Center (P30DK116074)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (26822)
- National Institutes of Health (/ NIDDK R01, ECCS-2026822, S10RR02557401, 1s10od032300-01, 1s10od010580-01a1, 1RO1AG060726)
- National Institute on Aging (R01AG060726)
- National Cancer Institute (R01CA204586, R01CA251155, R37CA214136, P30CA124435, R01CA277710, R01CA250227)
- National Institute of General Medical Sciences (R01GM126256, R35GM136226)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK083283, P30DK120531, P30DK116074, R01DK062277)
- National Center for Research Resources (1S10OD010580-01A1, S10RR02557401, 1S10OD010580)
- Division of Electrical, Communications and Cyber Systems (ECCS-2026822, 2026822)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Physical Sciences › Engineering › Biomedical Engineering › Elasticity and Material Modeling
- Keywords
- hepatocellular carcinoma, advanced glycation end products, type 2 diabetes, collagen structure, extracellular matrix stiffness, β-catenin signaling, collagen cross-links, beta1 integrin, YAP, mechanotransduction, cancer cell proliferation and invasion
- MeSH terms
- Receptor for Advanced Glycation End Products, Tensins, YAP-Signaling Proteins, Animals, Collagen, Computer Simulation, Diabetes Mellitus, Type 2, Elasticity, Extracellular Matrix, Carcinoma, Hepatocellular, Humans, Liver Cirrhosis, Liver Neoplasms, Neoplasm Invasiveness, Viscosity, Glycation End Products, Advanced, Disease Progression, Integrin beta1, Cell Proliferation, beta Catenin
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