Glycoconjugates tune the viscoelastic signature of mammary tumor progression

This preprint reports that in the MMTV-PyMT mouse model, glycoconjugate accumulation drives increased viscoelasticity during mammary tumor progression. Spatial microindentation shows that coupling between stiffness and viscoelasticity weakens in late carcinoma, and selective enzymatic degradation of sulfated glycosaminoglycans, mucins, or O/N-linked glycans each reduces viscoelasticity without changing stiffness. In vitro, raising matrix viscoelasticity drives MCF10A epithelial cells toward a malignant phenotype via FAK mechanosignaling. The authors propose viscoelasticity as an independent mechanical marker of breast cancer progression and provide a benchmark for replication in engineered models.