SWI/SNF component ARID1A restrains pancreatic neoplasia formation
Open accessAbstract
Objective: ARID1A is commonly mutated in pancreatic ductal adenocarcinoma (PDAC), but the functional effects of ARID1A mutations in the pancreas are unclear. Understanding the molecular mechanisms that drive PDAC formation may lead to novel therapies. Design: Concurrent conditional Arid1a deletion and Kras activation mutations were modelled in mice. Small-interfering RNA (siRNA) and CRISPR/Cas9 were used to abrogate ARID1A in human pancreatic ductal epithelial cells. Results: We found that pancreas-specific Arid1a loss in mice was sufficient to induce inflammation, pancreatic intraepithelial neoplasia (PanIN) and mucinous cysts. Concurrent Kras activation accelerated the development of cysts that resembled intraductal papillary mucinous neoplasm. Lineage-specific Arid1a deletion confirmed compartment-specific tumour-suppressive effects. Duct-specific Arid1a loss promoted dilated ducts with occasional cyst and PDAC formation. Heterozygous acinar-specific Arid1a loss resulted in accelerated PanIN and PDAC formation with worse survival. RNA-seq showed that Arid1a loss induced gene networks associated with Myc activity and protein translation. ARID1A knockdown in human pancreatic ductal epithelial cells induced increased MYC expression and protein synthesis that was abrogated with MYC knockdown. ChIP-seq against H3K27ac demonstrated an increase in activated enhancers/promoters. Conclusions: Arid1a suppresses pancreatic neoplasia in a compartment-specific manner. In duct cells, this process appears to be associated with MYC-facilitated protein synthesis.
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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 [99]
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Pancreatic cancer: Advances and challenges
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- Authors
- Wang, S. C., Nassour, I., Xiao, S., Zhang, S., Luo, X., Lee, J., Li, L., Sun, X., Nguyen, L. H., Chuang, J.-C., Peng, L., Daigle, S., Shen, J., & Zhu, H.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Howard Hughes Medical Institute (US)
- Epizyme (United States) (US)
- Stanford Medicine (US)
- Corresponding author
- Zhu, Hao
- ORCID
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2018-10-12
- Volume
- 68
- Issue
- 7
- Pages
- 1259-1270
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- PMC
- PMC6499717
- OpenAlex
- W2896987809
- Cited by
- 85
- References
- 59
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 8 · 2023: 12 · 2022: 14 · 2021: 14 · 2020: 11 · 2019: 9
- FWCI
- 3.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Gut (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Center for Advancing Translational Sciences
- ChiRhoClin
- Cancer Prevention and Research Institute of Texas
- National Cancer Institute
- American Cancer Society
- Burroughs Wellcome Fund
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- ARID1A, SWI/SNF complex, pancreatic ductal adenocarcinoma, pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm, KRAS activation, c-Myc, protein synthesis, pancreatic cysts, pancreatic ductal cells
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Disease Models, Animal, DNA-Binding Proteins, Humans, Nuclear Proteins, Pancreatic Neoplasms, Transcription Factors, Proto-Oncogene Proteins c-myc, Proto-Oncogene Proteins p21(ras), Cell Culture Techniques, Carcinoma, Pancreatic Ductal, Mice
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