A bright future for protein kinase D1 as a drug target to prevent or treat pancreatic cancer.
Pancreatic ductal adenocarcinoma originates from acinar cells that undergo acinar-to-ductal metaplasia (ADM). ADM is initiated in response to growth factors, inflammation, and oncogene activation and leads to a de-differentiated, duct-like phenotype. Our recent publication demonstrated a transforming growth factor α-Kras(G12D)-protein kinase D1-Notch1 signaling axis driving the induction of ADM and further progression to pancreatic intraepithelial neoplasia. This suggests that protein kinase D1 might be an early marker for tumor development and a potential target for drug development.
Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic , Jacksonville, FL, USA.
Geou-Yarh
GY
Liou
Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic , Jacksonville, FL, USA.
Peter
P
Storz
The Biotechnology Center of Oslo, University of Oslo , Oslo, Norway.
Michael
M
Leitges
Acinar-to-ductal metaplasia; mechanisms of oncogenesis and tumor progression; mouse model; oncogenic Kras; pancreatic cancer; protein kinase D1