Kruppel-like Factor 5, Increased in Pancreatic Ductal Adenocarcinoma, Promotes Proliferation, Acinar-to-Ductal Metaplasia, Pancreatic Intraepithelial Neoplasia, and Tumor Growth in Mice.

ABSTRACT:

Background & aims

Activating mutations in KRAS are detected in most pancreatic ductal adenocarcinomas (PDACs). Expression of an activated form of KRAS (KrasG12D) in pancreata of mice is sufficient to induce formation of pancreatic intraepithelial neoplasia (PanINs)-a precursor of PDAC. Pancreatitis increases formation of PanINs in mice that express KrasG12D by promoting acinar-to-ductal metaplasia (ADM). We investigated the role of the transcription factor Krüppel-like factor 5 (KLF5) in ADM and KRAS-mediated formation of PanINs.

Methods

We performed studies in adult mice with conditional disruption of Klf5 (Klf5^fl/fl) and/or expression of Kras^G12D (LSL-Kras^G12D) via Cre^ERTM recombinase regulated by an acinar cell-specific promoter

SUBMITTER: He P 

PROVIDER: S-EPMC5880723 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature