Growth Factors and Integrins (GF-Integrin Crosstalk)

Growth factors and integrins represent two major classes of cell surface receptors that cooperatively regulate fundamental cellular processes through bidirectional crosstalk. Growth factors, such as Vascular Endothelial Growth Factor (VEGF) and Transforming Growth Factor-beta (TGF-beta), typically signal through receptor tyrosine kinases (RTKs) to drive cell proliferation, differentiation, and survival (Ivaska & Heino, 2011, Nature Reviews Molecular Cell Biology). Integrins are heterodimeric transmembrane receptors that mediate cell-extracellular matrix (ECM) adhesion, providing the structural context necessary for growth factor signaling to occur efficiently. This synergy is often exploited in pathological states; for instance, integrins can physically associate with growth factor receptors to amplify oncogenic signaling, promoting tumor invasion and metastasis (Desgrosellier & Cheresh, 2010, Nature Reviews Cancer). In fibrosis, integrins like alpha-v-beta-6 are essential for the activation of latent TGF-beta, a master regulator of collagen deposition (Henderson & Sheppard, 2013, Nature). Therapeutic interventions targeting this axis include monoclonal antibodies that neutralize growth factor ligands or block specific integrin subunits to disrupt the pro-survival and pro-migratory environment of diseased tissues.

Other names

Growth factor-integrin signaling complexIntegrin-growth factor receptor interactionGF-Integrin axisCell-matrix and growth factor signaling

Inhibition of ligand binding to growth factor receptors or integrins, disruption of receptor-integrin physical association, and blockade of downstream intracellular signaling cascades such as the MAPK/ERK and PI3K/AKT pathways.