Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia
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Background & aims Invasive pancreatic ductal adenocarcinoma is thought to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN). PanINs progress from low grade (PanIN-1) to high grade (PanIN-3) as the cells attain molecular alterations to key regulatory genes, including activating mutations in the KRAS protooncogene. Despite a well-documented progression model, our knowledge of the initiator cells of PanINs and the transcriptional networks and signaling pathways that impact PanIN formation remains incomplete.Methods In this study, we examined the importance of the acinar-restricted transcription factor Mist1 to KrasG12D-induced mouse PanIN (mPanIN) formation in 3 different mouse models of pancreatic cancer.Results In the absence of Mist1 (Mist1KO), KrasG12D-expressing mice exhibited severe exocrine pancreatic defects that were rescued by ectopic expression of Mist1 in acinar cells. mPanIN development was greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO acinar cells were predisposed to convert to a ductal phenotype and activate epidermal growth factor receptor (EGFR) and Notch-signaling pathways.Conclusions We propose that convergence of EGFR, Notch, and Kras pathways in acinar cells lacking Mist1 leads to enhanced mPanIN formation.
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Heterozygous or homozygous deletion of terminal acinar differentiation factors Ptf1a, Mist1, and Nr5a2 accelerates KRAS-driven tumorigenesis.
“heterozygous or homozygous deletion of factors associated with terminal acinar differentiation such as Ptf1a, Mist1, and Nr5a2 accelerate KRAS-driven tumorigenesis119–122.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [121]
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Self-citation
- Authors
- Shi, G., Zhu, L., Sun, Y., Bettencourt, R., Damsz, B., Hruban, R. H., & Konieczny, S. F.
- Affiliations
- Purdue University West Lafayette (US)
- Johns Hopkins University (US)
- Corresponding author
- Konieczny, Stephen F.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 136
- Issue
- 4
- Pages
- 1368-1378
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC2845927
- OpenAlex
- W2123155461
- Cited by
- 168
- References
- 39
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 7 · 2023: 9 · 2022: 4 · 2021: 11 · 2020: 8 · 2019: 13 · 2018: 12 · 2017: 11 · 2016: 9 · 2015: 20 · 2014: 11 · 2013: 10 · 2012: 10
- FWCI
- 4.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Thurgood Marshall College Fund
- Lustgarten Foundation (P50CA62924)
- Purdue University
- National Institutes of Health
- National Cancer Institute (P50CA-62924, R01CA124586, CA124586, P50CA062924)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK55489, R01DK055489)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
- Keywords
- Mist1, pancreatic intraepithelial neoplasia, KRAS G12D, pancreatic ductal adenocarcinoma, acinar cells, pancreatic cancer progression, EGFR signaling, Notch signaling, transcription factors
- MeSH terms
- Animals, Carcinoma in Situ, Cell Transformation, Neoplastic, Cells, Cultured, Disease Models, Animal, Mice, Transgenic, Pancreatic Neoplasms, Signal Transduction, Proto-Oncogene Proteins p21(ras), Mice, Knockout, Disease Progression, Mice, Basic Helix-Loop-Helix Proteins, Receptors, Notch, ErbB Receptors
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