UBE2C promotes pancreatic tumorigenesis by KRAS stabilization via APC/CCDH1-mediated WDR76 degradation

This is the authors' abstract. We don't add key points for this paper.

and UBE2C increase. Furthermore, simultaneous WDR76 knockdown via adeno-associated virus (AAV) injection into the pancreatic duct fully rescues RAS/ERK inactivation and PDAC suppression caused by Ube2c deletion, demonstrating a causal role of the UBE2C-WDR76 axis. Collectively, these findings suggest that the UBE2C-WDR76 axis may represent a promising therapeutic target for the treatment of KRAS-driven pancreatic cancer.