Arp2/3 complex and β1 integrin drive an invasive front through extracellular matrix adaptation in pancreatic cancer - PubMed
4 days ago
- #Pancreatic Cancer
- #Cell Migration
- #Extracellular Matrix
- Pancreatic ductal adenocarcinoma (PDAC) is highly aggressive and resistant to therapy due to its invasive nature.
- The extracellular matrix (ECM), rich in collagen I, collagen IV, and laminin, acts as a mechanical barrier to PDAC invasion.
- The Arp2/3 complex, an actin nucleator, is crucial for PDAC cells to overcome ECM stiffness and facilitate migration.
- CRISPR/Cas9 knockout of Arpc4 in murine PDAC cells downregulated Arp2/3 complex members, impairing migration and invasive front formation.
- β1 integrin signaling regulates Arp2/3-dependent migration through collagen-rich matrices.
- High expression of Arp2/3 complex components correlates with poor patient survival and basal-like PDAC subtypes.
- Arp2/3 complex and β1 integrin are potential therapeutic targets for mitigating PDAC progression.