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The Cell–extracellular matrix (ECM) adhesion interface is a complex biological structure that facilitates physical attachment and biochemical communication between a cell and its surrounding matrix. This interface is primarily mediated by the integrin family of transmembrane receptors, which cluster into specialized sites known as focal adhesions or hemidesmosomes (Hynes, R. O., Cell, 2002; Geiger, B., et al., Nat Rev Mol Cell Biol, 2009). These structures act as mechanosensors, translating physical forces from the ECM into intracellular chemical signals that regulate essential processes such as cell survival, migration, and differentiation (Geiger, B., et al., Nat Rev Mol Cell Biol, 2009; Winograd-Katz, S. E., et al., Nat Rev Mol Cell Biol, 2014). In many diseases, including cancer and fibrosis, the Cell–ECM interface is dysregulated, promoting tumor invasion, metastasis, and pathological tissue remodeling (Desgrosellier, J. S., & Cheresh, D. A., Nat Rev Cancer, 2010). Therapeutic targeting of this interface typically involves small molecules or monoclonal antibodies designed to block integrin-ligand interactions, thereby disrupting the signaling and migratory capabilities of pathogenic cells (Winograd-Katz, S. E., et al., Nat Rev Mol Cell Biol, 2014; Desgrosellier, J. S., & Cheresh, D. A., Nat Rev Cancer, 2010).
Inhibition of integrin-mediated cell attachment to extracellular matrix components; blockade of outside-in and inside-out signaling pathways.
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