TBC1D23 drives lymphatic metastasis in pancreatic ductal adenocarcinoma by altering EGFR cell surface dynamics and signaling - PubMed
18 hours ago
- #Lymphangiogenesis
- #EGFR Signaling
- #PDAC
- TBC1D23 is identified as a novel oncogenic driver in pancreatic ductal adenocarcinoma (PDAC).
- Elevated TBC1D23 expression correlates with lymphatic metastasis and poor survival in PDAC patients.
- TBC1D23 depletion inhibits PDAC cell proliferation, migration, invasion, and tumor growth in vitro and in vivo.
- TBC1D23 regulates EGFR trafficking, enhancing recycling and membrane localization while suppressing degradation.
- TBC1D23 sustains EGFR/ERK signaling, leading to upregulation of VEGF-C and promoting lymphangiogenesis.
- VEGF-C supplementation rescues the effects of TBC1D23 depletion, and VEGFR3 inhibitor MAZ51 abolishes them.
- The study highlights TBC1D23 as a potential biomarker and therapeutic target for PDAC lymphatic metastasis.