CPT1A Over-Expression Increases Reactive Oxygen Species in the Mitochondria and Promotes Antioxidant Defenses in Prostate Cancer
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Cancers reprogram their metabolism to adapt to environmental changes. In this study, we examined the consequences of altered expression of the mitochondrial enzyme carnitine palmitoyl transferase I (CPT1A) in prostate cancer (PCa) cell models. Using transcriptomic and metabolomic analyses, we compared LNCaP-C4-2 cell lines with depleted (knockdown (KD)) or increased (overexpression (OE)) CPT1A expression. Mitochondrial reactive oxygen species (ROS) were also measured. Transcriptomic analysis identified ER stress, serine biosynthesis and lipid catabolism as significantly upregulated pathways in the OE versus KD cells. On the other hand, androgen response was significantly downregulated in OE cells. These changes associated with increased acyl-carnitines, serine synthesis and glutathione precursors in OE cells. Unexpectedly, OE cells showed increased mitochondrial ROS but when challenged with fatty acids and no androgens, the Superoxide dismutase 2 (SOD2) enzyme increased in the OE cells, suggesting better antioxidant defenses with excess CPT1A expression. Public databases also showed decreased androgen response correlation with increased serine-related metabolism in advanced PCa. Lastly, worse progression free survival was observed with increased lipid catabolism and decreased androgen response. Excess CPT1A is associated with a ROS-mediated stress phenotype that can support PCa disease progression. This study provides a rationale for targeting lipid catabolic pathways for therapy in hormonal cancers.
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Gain and loss of function of CPT1A elucidated genetic and metabolic vulnerabilities in prostate cancer.
“Another study applied gain and loss of function of CPT1A, which encodes a fatty acids metabolism enzyme, to elucidate genetic and metabolic vulnerabilities in prostate cancer158.”
From The technological landscape and applications of single-cell multi-omics (2023) · cites this paper as [158]
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- Authors
- Joshi, M., Kim, J., D’Alessandro, A., Monk, E., Bruce, K., Elajaili, H., Nozik-Grayck, E., Goodspeed, A., Costello, J. C., & Schlaepfer, I. R.
- Affiliations
- University of Colorado Anschutz (US)
- University of Colorado Cancer Center (US)
- Department of Pediatrics Critical Care, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
- Corresponding author
- Schlaepfer, Isabel R.
- ORCID
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2020-11-18
- Volume
- 12
- Issue
- 11
- Pages
- 3431
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC7709014
- OpenAlex
- W3105277425
- Cited by
- 54
- References
- 64
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 15 · 2023: 7 · 2022: 8 · 2021: 7
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Cancer Society (129846-RSG-16-256)
- National Institutes of Health (P30CA046934 and CA231978)
- Cancer League of Colorado (AWD-193286)
- Nutrition and Obesity Research Center (Sept2020)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Keywords
- CPT1A, prostate cancer, mitochondrial reactive oxygen species, antioxidant defense, manganese superoxide dismutase, androgen response, serine biosynthesis, lipid degradation, endoplasmic reticulum stress, acylcarnitines, glutathione precursor, cancer metabolism, progression-free survival
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