Pancreatic STAT5 activation promotes Kras^G12D-induced and inflammation-induced acinar-to-ductal metaplasia and pancreatic cancer.

ABSTRACT:

Objective

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy because it is often diagnosed at a late-stage. Signal transducer and activator of transcription 5 (STAT5) is a transcription factor implicated in the progression of various cancer types. However, its role in KRAS-driven pancreatic tumourigenesis remains unclear.

Design

We performed studies with LSL-Kras ^G12D; Ptf1a-Cre ^ERT (KC^ERT) mice or LSL-Kras^G12D; LSL-Trp53^R172H ; Pdx1-Cre (KPC) mice crossed with conditional disruption of STAT5 or completed deficiency interleukin (IL)-22. Pancreatitis was induced in mice by administration of cerulein. Pharmacological inhibition of STAT5 on PDAC prevention was studied in the or

SUBMITTER: Lin Y 

PROVIDER: S-EPMC11503187 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature