C-Jun N-terminal kinase in pancreatic tumor stroma augments tumor development in mice.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a life-threatening disease and there is an urgent need to develop improved therapeutic approaches. The role of c-Jun N-terminal kinase (JNK) in PDAC stroma is not well defined even though dense desmoplastic reactions are characteristic of PDAC histology. We aimed to explore the role of JNK in PDAC stroma in mice. We crossed Ptf1a^Cre/+ ;Kras^G12D/+ mice with JNK1^-/- mice to generate Ptf1a^Cre/+ ;Kras^G12D/+ ;JNK1^-/- (Kras;JNK1^-/- ) mice. Tumor weight was significantly lower in Kras;JNK1^-/- mice than in Kras;JNK1^+/- mice, whereas histopathological features were similar. We also transplanted a murine PDAC cell line (mPC) with intact JNK1 s.c. into WT and J

SUBMITTER: Sato T 

PROVIDER: S-EPMC5666025 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature