Paradoxical Role of AT-rich Interactive Domain 1A in Restraining Pancreatic Carcinogenesis
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Abstract
Background & Aims: ARID1A is postulated to be a tumor suppressor gene owing to loss-of-function mutations in human pancreatic ductal adenocarcinomas (PDAC). However, its role in pancreatic pathogenesis is not clear despite recent studies using genetically engineered mouse (GEM) models. We aimed at further understanding of its direct functional role in PDAC, using a combination of GEM model and PDAC cell lines. Methods: Pancreas-specific mutant Arid1a-driven GEM model (Ptf1a-Cre; KrasG12D; Arid1af/f or “KAC”) was generated by crossing Ptf1a-Cre; KrasG12D (“KC”) mice with Arid1af/f mice and characterized histologically with timed necropsies. Arid1a was also deleted using CRISPR-Cas9 system in established human and murine PDAC cell lines to study the immediate effects of Arid1a loss in isogenic models. Cell lines with or without Arid1a expression were developed from respective autochthonous PDAC GEM models, compared functionally using various culture assays, and subjected to RNA-sequencing for comparative gene expression analysis. DNA damage repair was analyzed in cultured cells using immunofluorescence and COMET assay. Results: Retention of Arid1a is critical for early progression of mutant Kras-driven pre-malignant lesions into PDAC, as evident by lower Ki-67 and higher apoptosis staining in “KAC” as compared to “KC” mice. Enforced deletion of Arid1a in established PDAC cell lines caused suppression of cellular growth and migration, accompanied by compromised DNA damage repair. Despite early development of relatively indolent cystic precursor lesions called intraductal papillary mucinous neoplasms (IPMNs), a subset of “KAC” mice developed aggressive PDAC in later ages. PDAC cells obtained from older autochthonous “KAC” mice revealed various compensatory (“escaper”) mechanisms to overcome the growth suppressive effects of Arid1a loss. Conclusions: Arid1a is an essential survival gene whose loss impairs cellular growth, and thus, its expression is critical during early stages of pancreatic tumorigenesis in mouse models. In tumors that arise in the setting of ARID1A loss, a multitude of “escaper” mechanisms drive progression.
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Context-specific tumor suppressive or oncogenic functions of SWI/SNF chromatin regulation have been noticed in PDAC.
“Context-specific tumor suppressive or oncogenic functions of SWI/SNF chromatin regulation was noticed in PDAC64,65.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [65]
Chromatin regulatory factors may have context-specific and biphasic functions in PDAC, with both tumor suppressor and oncogenic roles at distinct stages of tumorigenesis.
“chromatin regulatory factors may have a more context-specific and biphasic function in PDAC, with studies in autochthonous models suggesting both tumor suppressor and oncogenic functions during distinct stages of tumorigenesis101,102.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [102]
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- Authors
- Ferri-Borgogno, S., Barui, S., McGee, A. M., Griffiths, T., Singh, P. K., Piett, C. G., Ghosh, B., Bhattacharyya, S., Singhi, A., Pradhan, K., Verma, A., Nagel, Z., Maitra, A., & Gupta, S.
- Affiliations
- Department of Translational Molecular Pathology and Sheikh Ahmed Center for Pancreatic Cancer Research, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
- The University of Texas MD Anderson Cancer Center (US)
- Harvard University (US)
- Albert Einstein College of Medicine (US)
- University of Pittsburgh Medical Center (US)
- Corresponding author
- Maitra, Anirban
- Gupta, Sonal
- ORCID
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2020-09-21
- Volume
- 12
- Issue
- 9
- Pages
- 2695
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC7564752
- OpenAlex
- W3087468412
- Cited by
- 22
- References
- 57
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 7 · 2022: 2 · 2021: 4 · 2020: 1
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- D-Scholarship@Pitt (University of Pittsburgh) (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Cancer Institute (P01 CA117969, R01 CA218004, R01 CA220236, U24 CA224020)
- 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, pancreatic ductal adenocarcinoma, pancreatic carcinogenesis, tumor suppressor, KRAS G12D, intraductal papillary mucinous neoplasm, DNA repair, tumor progression, pancreatic precancerous lesions
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