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Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis
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Abstract
Pancreatic ductal adenocarcinoma (PDA) has a poor prognosis, and new strategies for prevention and treatment are urgently needed. We previously reported that histone H4 acetylation is elevated in pancreatic acinar cells harboring Kras mutations prior to the appearance of premalignant lesions. Because acetyl-CoA abundance regulates global histone acetylation, we hypothesized that altered acetyl-CoA metabolism might contribute to metabolic or epigenetic alterations that promote tumorigenesis. We found that acetyl-CoA abundance is elevated in KRAS-mutant acinar cells and that its use in the mevalonate pathway supports acinar-to-ductal metaplasia (ADM). Pancreas-specific loss of the acetyl-CoA–producing enzyme ATP-citrate lyase (ACLY) accordingly suppresses ADM and tumor formation. In PDA cells, growth factors promote AKT–ACLY signaling and histone acetylation, and both cell proliferation and tumor growth can be suppressed by concurrent BET inhibition and statin treatment. Thus, KRAS-driven metabolic alterations promote acinar cell plasticity and tumor development, and targeting acetyl-CoA–dependent processes exerts anticancer effects. Significance: Pancreatic cancer is among the deadliest of human malignancies. We identify a key role for the metabolic enzyme ACLY, which produces acetyl-CoA, in pancreatic carcinogenesis. The data suggest that acetyl-CoA use for histone acetylation and in the mevalonate pathway facilitates cell plasticity and proliferation, suggesting potential to target these pathways. See related commentary by Halbrook et al., p. 326. This article is highlighted in the In This Issue feature, p. 305
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“Oncogenic KRas increases the levels of acetyl coenzyme A (CoA) and reactive oxygen species (ROS) before the development of ADM, and inhibiting these phenotypes blocks ADM (19, 20).”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [20]
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Metadata
- Authors
- Carrer, A., Trefely, S., Zhao, S., Campbell, S. L., Norgard, R. J., Schultz, K. C., Sidoli, S., Parris, J. L. D., Affronti, H. C., Sivanand, S., Egolf, S., Sela, Y., Trizzino, M., Gardini, A., Garcia, B. A., Snyder, N. W., Stanger, B. Z., & Wellen, K. E.
- Affiliations
- University of Pennsylvania (US)
- Drexel University (US)
- The Wistar Institute (US)
- Corresponding author
- Wellen, Kathryn E.
- ORCID
- Venue
- Cancer Discovery
- Published
- 2019-03-01
- Volume
- 9
- Issue
- 3
- Pages
- 416-435
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC6643997
- OpenAlex
- W2911157836
- Cited by
- 313
- References
- 76
- Citations by year
- 2026: 23 · 2025: 49 · 2024: 62 · 2023: 47 · 2022: 44 · 2021: 42 · 2020: 31 · 2019: 15
- FWCI
- 10.44
- Type
- journal article
- Language
- en
- Update notices
- correction (2024-09-04)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- Pancreatic Cancer Action Network (14-20-25-WELL)
- NIH (R01CA174761, R01CA228339, R03HD092630, GM110174, AI118891, CA196539, 1F31CA217070-01, F99CA222741, 4K00CA212455-03)
- American Diabetes Association (#1-18-PDF-144)
- UPenn Baccalaureate Research Education (R25-GM071745)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- acetyl-CoA metabolism, pancreatic ductal adenocarcinoma, pancreatic carcinogenesis, ATP citrate lyase, histone H4 acetylation, acinar-to-ductal metaplasia, KRAS mutation, mevalonate pathway, Akt signaling, BET inhibition, statins, cellular plasticity, epigenetic regulation, pancreatic acinar cells
- MeSH terms
- Acetyl Coenzyme A, Acetylation, Animals, Female, Histones, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Pancreatic Neoplasms, Protein Processing, Post-Translational, Genes, ras, Signal Transduction, Mice, Knockout, Carcinoma, Pancreatic Ductal, Cell Proliferation, Acinar Cells, Carcinogenesis, Heterografts
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