CREB drives acinar cells to ductal reprogramming and promotes pancreatic cancer progression in preclinical models of alcoholic pancreatitis.

ABSTRACT:

Background & aims

Chronic alcoholism often leads to pancreatitis, which exacerbates pancreatic damage through acinar cell injury, fibrotic inflammation and activates AKT/mTOR/cyclic adenosine monophosphate response element binding protein 1 (CREB) signaling axis. However, the molecular interplay between oncogenic Kras ^G12D/+(Kras*) and CREB in promoting pancreatic cancer progression under chronic inflammation remains poorly understood.

Methods

Experimental alcoholic chronic pancreatitis (ACP) induction was established in multiple mouse models, with euthanasia during the recovery stage to evaluate tumor latency. CREB was selectively deleted (Creb^fl/fl ) in Ptf1a^CreERTM/+;LSL-Kras^G12D/+ (KC)

SUBMITTER: Srinivasan S 

PROVIDER: S-EPMC11188065 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature