“…During the oncogenic transformation, the ECM ligand binding activity is regulated by changing various parameters, such as extracellular and intracellular ligands, e.g., the proteoglycan decorin or intracellular kindlins, as well as divalent cations and protons, redox-active compounds, and mechanical forces [ 82 , 100 , 101 , 102 , 103 , 104 , 105 ]. Therefore, integrin expression and surface abundance on cancer cells can serve as tumor (suppressor) markers, although this may vary between tumor entities [ 91 , 106 , 107 , 108 ]. For example, the expression of α3β1 and α11β1 integrins changes during CAF differentiation, whereupon CAFs interact via these integrins with ectopically expressed laminin-332 and desmoplastically abundant collagen, respectively, and thus support cancer cells [ 24 , 109 ].…”