The chromatin regulator Brg1 suppresses formation of intraductal papillary mucinous neoplasm and pancreatic ductal adenocarcinoma
Open accessAbstract
Pancreatic ductal adenocarcinoma (PDA) develops through distinct precursor lesions, including pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasia (IPMN). However, genetic features resulting in IPMN-associated PDA (IPMN-PDA) versus PanIN-associated PDA (PanIN-PDA) are largely unknown. Here we find that loss of Brg1, a core subunit of SWI/SNF chromatin remodelling complexes, cooperates with oncogenic Kras to form cystic neoplastic lesions that resemble human IPMN and progress to PDA. Although Brg1-null IPMN-PDA develops rapidly, it possesses a distinct transcriptional profile compared with PanIN-PDA driven by mutant Kras and hemizygous p53 deletion. IPMN-PDA also is less lethal, mirroring prognostic trends in PDA patients. In addition, Brg1 deletion inhibits Kras-dependent PanIN development from adult acinar cells, but promotes Kras-driven preneoplastic transformation in adult duct cells. Therefore, this study implicates Brg1 as a determinant of context-dependent Kras-driven pancreatic tumorigenesis and suggests that chromatin remodelling may underlie the development of distinct PDA subsets.
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Deletion of SWI/SNF factors Arid1a or Brg1 accelerates pancreatic tumorigenesis on a backdrop of cystic neoplasms resembling human IPMNs.
“deletion of SWI/SNF factors Arid1a or Brg1 results in the acceleration of pancreatic tumorigenesis on the backdrop of cystic neoplasms resembling human IPMNs98–100.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [100]
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- Authors
- von Figura, G., Fukuda, A., Roy, N., Liku, M. E., Morris IV, J. P., Kim, G. E., Russ, H. A., Firpo, M. A., Mulvihill, S. J., Dawson, D. W., Ferrer, J., Mueller, W. F., Busch, A., Hertel, K. J., & Hebrok, M.
- Affiliations
- University of California, San Francisco (US)
- University of Utah (US)
- University of California, Los Angeles (US)
- Imperial College London (GB)
- University of California, Irvine (US)
- Corresponding author
- Hebrok, Matthias
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2014-02-23
- Volume
- 16
- Issue
- 3
- Pages
- 255-267
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC4684081
- OpenAlex
- W1970847274
- Cited by
- 190
- References
- 62
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 9 · 2023: 11 · 2022: 12 · 2021: 15 · 2020: 19 · 2019: 19 · 2018: 19 · 2017: 21 · 2016: 23 · 2015: 20 · 2014: 7
- FWCI
- 11.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Funders
- Wellcome Trust (101033, 101033/C/13/Z)
- Deutsche Forschungsgemeinschaft (FI 1719/1-1)
- National Institutes of Health
- U.S. Public Health Service (TG2 01153)
- University of California, San Francisco
- Japan Society for the Promotion of Science
- National Cancer Institute (CA112537, CA149548, P01CA163200, R01CA112537, R21CA149548, P30CA062203)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30-DK-63720, P30DK063720)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
- Keywords
- SMARCA4, SWI/SNF chromatin remodeling, intraductal papillary mucinous neoplasm, pancreatic ductal adenocarcinoma, pancreatic intraepithelial neoplasia, pancreatic carcinogenesis, p53 deletion, gene expression profiling, acinar cells, duct cells, mouse model
- MeSH terms
- Animals, Adenocarcinoma, Mucinous, DNA Helicases, Female, Humans, Male, Mice, Transgenic, Nuclear Proteins, Pancreas, Pancreatic Neoplasms, Transcription Factors, Proto-Oncogene Proteins p21(ras), Mice, SCID, Mice, Inbred NOD, Carcinoma, Pancreatic Ductal, Chromatin Assembly and Disassembly, Cell Line, Tumor, Cell Proliferation, Mice, Carcinogenesis
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