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Cell migration involves a dynamic cycle of integrin assembly and disassembly, which is crucial for embryonic development, immune defense, and tissue repair. Recent studies have identified the upregulation of α₅β₁ integrin (INTG) as a facilitator of tumor initiation in pancreatic cancer cells. To elucidate the mechanisms underlying tumor initiation and metastasis through integrin-ECM interactions, α₅β₁ INTG is overexpressed in human dermal fibroblasts using recombinant lentiviruses. Utilizing super-resolution microscopy, four distinct integrin clustering types are categorized, and the morphology and length distribution are analyzed in the presence and absence of fibronectin. Our findings indicate that α₅β₁ overexpressing (OE) cells undergo distinct dynamic alterations in integrin clustering compared to normal cells. The α₅β₁ OE cells demonstrate an increased spreading area, which affects fibronectin engagement and promotes enhanced fibrillogenesis. Moreover, the strong interaction between α₅β₁ OE cells and fibronectin, as well as with other overexpressing cells, leads to the formation of fibronectin-rich niches, which are characteristic of tumor-initiating or metastatic microenvironments.

α5β1 Integrin; fibronectin; extracellular matrix; tumor