ITGA5 (integrin subunit alpha 5) is a cell adhesion molecule that mediates integrin-mediated signaling through formation of the integrin alpha5-beta1 complex and focal adhesion assembly 1. ITGA5 activates downstream FAK/PI3K/AKT signaling pathways critical for cell-substrate interactions 2. Mechanistically, ITGA5 can be regulated post-transcriptionally through miRNA sponging and competitive endogenous RNA mechanisms, and its protein stability is modulated by N-glycosylation affecting exosomal trafficking 3. In cancer contexts, ITGA5 promotes aggressive phenotypes across multiple malignancies. In triple-negative breast cancer, ITGA5 expression is upregulated through the circRPPH1/miR-326 axis and drives FAK/Src signaling-dependent chemoresistance 12. In glioblastoma, ITGA5 stabilization in mesenchymal cells facilitates tumor-macrophage interactions promoting immune evasion; blocking ITGA5 potentiates anti-PD-1 therapy 3. In hepatocellular carcinoma, myofibroblast-derived extracellular vesicles transfer ITGA5 to tumor cells, enhancing cancer stem cell properties through YES1 activation 4. Beyond cancer, ITGA5+ synovial fibroblasts promote rheumatoid arthritis progression by inducing pathogenic T helper cell differentiation 5. ITGA5-mediated fibronectin signaling also regulates fibrosis through macrophage reprogramming 6. Therapeutically, ITGA5 blockade emerges as a promising strategy across multiple diseases by disrupting pro-pathogenic cell interactions and signaling cascades.