Warfarin and bevacizumab suppress tumor progression in pancreatic ductal adenocarcinoma by targeting EGFR-PI3K-Akt signaling: inhibition of proliferation/migration and apoptosis induction.

ABSTRACT:

Background

Pancreatic ductal adenocarcinoma (PDAC) exhibits aggressive progression, dense stromal remodeling, and resistance to chemotherapy, resulting in extremely poor survival. Although bevacizumab-mediated vascular endothelial growth factor (VEGF) inhibition can suppress angiogenesis, clinical efficacy is limited by compensatory activation of alternative signaling pathways. Meanwhile, PDAC-associated hypercoagulability supports tumor progression, and warfarin has been reported to exert anti-tumor effects partly through inhibition of the growth arrest-specific protein 6 (Gas6)/Axl-phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt) axis. Given that epidermal growth factor receptor (EGFR) also converges on the PI3K-Akt pathway, combining warfarin with bevacizumab may enhance

SUBMITTER: Chen J 

PROVIDER: S-EPMC12776193 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature