The acinar differentiation determinant PTF1A inhibits initiation of pancreatic ductal adenocarcinoma
Open accessAbstract
Understanding the initiation and progression of pancreatic ductal adenocarcinoma (PDAC) may provide therapeutic strategies for this deadly disease. Recently, we and others made the surprising finding that PDAC and its preinvasive precursors, pancreatic intraepithelial neoplasia (PanIN), arise via reprogramming of mature acinar cells. We therefore hypothesized that the master regulator of acinar differentiation, PTF1A, could play a central role in suppressing PDAC initiation. In this study, we demonstrate that PTF1A expression is lost in both mouse and human PanINs, and that this downregulation is functionally imperative in mice for acinar reprogramming by oncogenic KRAS. Loss of Ptf1a alone is sufficient to induce acinar-to-ductal metaplasia, potentiate inflammation, and induce a KRAS-permissive, PDAC-like gene expression profile. As a result, Ptf1a -deficient acinar cells are dramatically sensitized to KRAS transformation, and reduced Ptf1a greatly accelerates development of invasive PDAC. Together, these data indicate that cell differentiation regulators constitute a new tumor suppressive mechanism in the pancreas.
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Loss of master regulators, such as Pax5 in B cells, can cause plasticity and even cancer.
“Their loss, for example, Pax5 in B cells, can cause plasticity and even cancer6,7,55,56.”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [7]
The Abstract and Results report that loss of the acinar differentiation regulator PTF1A promotes cellular reprogramming and increases susceptibility to KRAS-driven pancreatic cancer. The paper does not address the sentence’s specific example of Pax5 loss in B cells; that part is not supported by this source. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredHeterozygous 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 [122]
Stabilized expression of PTF1A and MIST1 inhibits PanIN formation in the context of mutant KRAS expression.
“stabilized expression of PTF1A and MIST1 inhibit PanIN formation in the context of mutant KRAS expression122,123.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [122]
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- Authors
- Krah, N. M., De La O, J.-P., Swift, G. H., Hoang, C. Q., Willet, S. G., Chen Pan, F., Cash, G. M., Bronner, M. P., Wright, C. V., MacDonald, R. J., & Murtaugh, L. C.
- Affiliations
- University of Utah (US)
- Department of Human Genetics, University of Utah, Salt Lake City, United States
- The University of Texas Southwestern Medical Center (US)
- Vanderbilt University Medical Center (US)
- Department of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, United States
- Corresponding author
- Murtaugh, L Charles
- ORCID
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2015-07-07
- Volume
- 4
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC4536747
- OpenAlex
- W2165793228
- Cited by
- 166
- References
- 84
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 17 · 2023: 18 · 2022: 17 · 2021: 15 · 2020: 15 · 2019: 16 · 2018: 24 · 2017: 11 · 2016: 13 · 2015: 5
- FWCI
- 7.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Cancer Institute (R21-CA179453, F30-CA192819)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK061220, P01-DK42502)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32-HD007491)
- 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
- Ptf1a, pancreatic ductal adenocarcinoma, pancreatic intraepithelial neoplasia, acinar differentiation, acinar-to-ductal metaplasia, tumor suppression, inflammation, tumor initiation
- MeSH terms
- Adenocarcinoma, Animals, Carcinoma in Situ, Disease Models, Animal, Humans, Transcription Factors, Gene Expression Profiling, Carcinoma, Pancreatic Ductal, Mice, Cell Transdifferentiation, Acinar Cells
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