TP63-mediated enhancer reprogramming drives the squamous subtype of pancreatic ductal adenocarcinoma
Open accessAbstract
The aberrant expression of squamous lineage markers in pancreatic ductal adenocarcinoma (PDA) has been correlated with poor clinical outcomes. However, the functional role of this putative transdifferentiation event in PDA pathogenesis remains unclear. Here, we show that expression of the transcription factor TP63 (ΔNp63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo. This process ultimately leads to a powerful addiction of squamous PDA cells to continuous TP63 expression. Our study demonstrates the functional significance of squamous transdifferentiation in PDA and reveals TP63-based reprogramming as an experimental tool for investigating mechanisms and vulnerabilities linked to this aberrant cell fate transition.
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TP63 can promote more aggressive PDAC subtypes and can be induced by KDM6A loss.
“several candidate regulators such as TP63136, which can be induced by KDM6A loss97, can promote more aggressive subtypes”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [136]
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Dynamic Interactions of Transcription Factors and Enhancer Reprogramming in Cancer Progression
Zboril, E. K., Yoo, H., Chen, L., & Liu, Z. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.753051 · Cited by 18 · see citing works
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Pandey, S., Gupta, V. K., & Lavania, S. (2023) · Epigenomics · doi:10.2217/epi-2022-0177 · Cited by 17 · see citing works
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Ramal, M., Corral, S., Kalisz, M., Lapi, E., & Real, F. X. (2023) · Oncogene · doi:10.1038/s41388-023-02876-3 · Cited by 17 · see citing works
Interaction between MED12 and ΔNp63 activates basal identity in pancreatic ductal adenocarcinoma
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Self-citationDisruption of Broad Epigenetic Domains in PDAC Cells by HAT Inhibitors
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A STAT3/integrin axis accelerates pancreatic cancer initiation and progression
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Self-citation
- Authors
- Somerville, T. D. D., Xu, Y., Miyabayashi, K., Tiriac, H., Cleary, C. R., Maia-Silva, D., Milazzo, J. P., Tuveson, D. A., & Vakoc, C. R.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Corresponding author
- Vakoc, Christopher R.
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-11
- Volume
- 25
- Issue
- 7
- Pages
- 1741-1755.e7
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC6296757
- OpenAlex
- W2901608487
- Cited by
- 225
- References
- 83
- Citations by year
- 2026: 29 · 2025: 21 · 2024: 31 · 2023: 35 · 2022: 21 · 2021: 43 · 2020: 28 · 2019: 16 · 2018: 1
- FWCI
- 8.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Europe PMC (PubMed Central) (acceptedVersion, other-oa)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- New York State Library (C150158)
- American Association for Cancer Research (16-20-25-VAKO)
- Pershing Square Sohn Cancer Research Alliance
- Medical School, University of Michigan
- National Cancer Institute (5P01CA013106-Project)
- National Institutes of Health
- Center for Outcomes Research and Evaluation, Yale School of Medicine
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- p63, ΔNp63, pancreatic ductal adenocarcinoma, enhancer reprogramming, tumor cell motility, tumor invasion, metastasis, cell fate transitions
- MeSH terms
- Animals, Carcinoma, Squamous Cell, Enhancer Elements, Genetic, Humans, Phenotype, Transcription Factors, Transcription, Genetic, Genome, Human, Gene Expression Regulation, Neoplastic, Carcinoma, Pancreatic Ductal, Tumor Suppressor Proteins, Cell Line, Tumor, Mice, Carcinogenesis
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