Abstract:
:The transdifferentiation of pancreatic acinar cells to a ductal phenotype (acinar-to-ductal metaplasia, ADM) occurs after injury or inflammation of the pancreas and is a reversible process. However, in the presence of activating Kras mutations or persistent epidermal growth factor receptor (EGF-R) signalling, cells that underwent ADM can progress to pancreatic intraepithelial neoplasia (PanIN) and eventually pancreatic cancer. In transgenic animal models, ADM and PanINs are initiated by high-affinity ligands for EGF-R or activating Kras mutations, but the underlying signalling mechanisms are not well understood. Here, using a conditional knockout approach, we show that protein kinase D1 (PKD1) is sufficient to drive the reprogramming process to a ductal phenotype and progression to PanINs. Moreover, using 3D explant culture of primary pancreatic acinar cells, we show that PKD1 acts downstream of TGFα and Kras, to mediate formation of ductal structures through activation of the Notch pathway.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Liou GY,Döppler H,Braun UB,Panayiotou R,Scotti Buzhardt M,Radisky DC,Crawford HC,Fields AP,Murray NR,Wang QJ,Leitges M,Storz Pdoi
10.1038/ncomms7200subject
Has Abstractpub_date
2015-02-20 00:00:00pages
6200issn
2041-1723pii
ncomms7200journal_volume
6pub_type
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