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Journal article

Ciliogenesis and Hedgehog signalling are suppressed downstream of KRAS during acinar-ductal metaplasia in mouse

Abstract:
Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related deaths worldwide, but has a 5-year survival rate of only 7% primarily due to late diagnosis and ineffective therapies. To treat or even prevent PDAC, it is vital that we understand the initiating events that lead to tumour onset. PDAC develops from preneoplastic lesions, most commonly pancreatic intraepithelial neoplasias (PanINs), driven by constitutive activation of KRAS. In patients, PanINs are associated with regions of acinar-to-ductal metaplasia (ADM) where, in response to inflammation, acini dedifferentiate to a pancreatic progenitor-like fate. In healthy tissue this process is reversible leading to regeneration of the pancreas; however, in the presence of oncogenic KRAS, regeneration is blocked and ADM can give rise to PanIN lesions. Here, we used a 3D mouse acinar culture that recapitulates ADM in vitro to explore how KRAS prevents regeneration. Regeneration is regulated by Hedgehog (Hh) signalling, which is transduced via the primary cilium. In wild-type acini, cilia assemble upon ADM and Hh target gene expression is upregulated; however, ciliogenesis and Hh signalling are suppressed during ADM in cells expressing oncogenic KRAS. We show that ciliogenesis fails due to ectopic activation of the cilium disassembly pathway, which is mediated by AurkA, a direct transcriptional target of KRAS. Inhibition of AurkA is able to rescue primary cilia and restore Hh signalling. We suggest that this could be used as a mechanism to prevent the formation of early lesions and thereby prevent progression to PDAC.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1242/dmm.044289

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Oncology
Role:
Author
ORCID:
0000-0003-0297-8558
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Oncology
Role:
Author
ORCID:
0000-0002-5800-1220
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Oncology
Role:
Author
ORCID:
0000-0002-0060-6278


Publisher:
The Company of Biologists
Journal:
Disease Models and Mechanisms More from this journal
Volume:
2020
Issue:
13
Article number:
dmm044289
Publication date:
2020-06-22
Acceptance date:
2020-06-11
DOI:
EISSN:
1754-8411
ISSN:
1754-8403
Pmid:
32571902


Language:
English
Keywords:
Pubs id:
1115364
Local pid:
pubs:1115364
Deposit date:
2020-07-06

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