Matrix viscoelasticity promotes liver cancer progression in the pre-cirrhotic liver Type 2 diabetes mellitus (T2DM) is a major risk factor for hepatocellular carcinoma (HCC). Changes in extracellular matrix (ECM) mechanics contribute to cancer development, and increased stiffness is known to promote HCC progression in cirrhotic conditions. T2DM 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. T2DM and obesity are important risks for HCC, and it is estimated that up to 30% of HCCs in non-alcoholic steatohepatitis (NASH) occur at a precirrhotic stage when matrix stiffness is still low, and these patients often have poor glycaemic control. AGEs are produced by the non-enzymatic glycation of serum or tissue proteins during T2DM or can be ingested through the consumption of food prepared at high temperatures. Over time, AGEs accumulate in the matrix due to decreased clearance and metabolism and can biochemically modify collagen and ECM proteins. Although AGEs in NASH do not appear to increase stiffness greatly, they could affect ECM viscoelasticity. Tissues and ECMs are generally viscoelastic, exhibiting viscous energy dissipation in response to mechanical perturbations and a time-dependent mechanical response, such as stress relaxation in response to deformation. Recent research has shown that changes in ECM viscoelasticity, independent of stiffness, have impacted cell behaviours, including proliferation and migration of breast cancer cells. Viscoelasticity can modulate tissue growth dynamics, symmetry and the growth of cancer cells. Here we investigated the role of AGE-mediated changes in ECM mechanical properties on NASH and HCC progression. AGEs enhance liver visMatrix viscoelasticity promotes liver cancer progression in the pre-cirrhotic liver Type 2 diabetes mellitus (T2DM) is a major risk factor for hepatocellular carcinoma (HCC). Changes in extracellular matrix (ECM) mechanics contribute to cancer development, and increased stiffness is known to promote HCC progression in cirrhotic conditions. T2DM 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. T2DM and obesity are important risks for HCC, and it is estimated that up to 30% of HCCs in non-alcoholic steatohepatitis (NASH) occur at a precirrhotic stage when matrix stiffness is still low, and these patients often have poor glycaemic control. AGEs are produced by the non-enzymatic glycation of serum or tissue proteins during T2DM or can be ingested through the consumption of food prepared at high temperatures. Over time, AGEs accumulate in the matrix due to decreased clearance and metabolism and can biochemically modify collagen and ECM proteins. Although AGEs in NASH do not appear to increase stiffness greatly, they could affect ECM viscoelasticity. Tissues and ECMs are generally viscoelastic, exhibiting viscous energy dissipation in response to mechanical perturbations and a time-dependent mechanical response, such as stress relaxation in response to deformation. Recent research has shown that changes in ECM viscoelasticity, independent of stiffness, have impacted cell behaviours, including proliferation and migration of breast cancer cells. Viscoelasticity can modulate tissue growth dynamics, symmetry and the growth of cancer cells. Here we investigated the role of AGE-mediated changes in ECM mechanical properties on NASH and HCC progression. AGEs enhance liver vis