ArticleCancers2020
CPT1A Over-Expression Increases Reactive Oxygen Species in the Mitochondria and Promotes Antioxidant Defenses in Prostate Cancer.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Dual-functional Green Tea Polyphenol loaded Chitosan Nanoparticles for Eradication of Uropathogenic Biofilm and Induction of Apoptotic Pathways in Prostate Cancer Cells.Applied biochemistry and biotechnology · 2026Article
- PLIN1 restoration modulates lipid reprogramming and impedes tumor growth in ovarian cancer.BMC cancer · 2026Article
- Hypoxic microenvironment in cancer: role in metabolic reprogramming.Frontiers in oncology · 2026Review
- Systemic immune dysregulation in hypertensive disorders of pregnancy persists years after delivery.Frontiers in immunology · 2026Article
- Article
- The emerging metabolic role and treatment target of CPT1A in CRC.Frontiers in cell and developmental biology · 2026Review
- Systemic immune dysregulation in hypertensive disorders of pregnancy persists years after delivery.bioRxiv : the preprint server for biology · 2025Article
- Carnitine Shuttle and Ferroptosis in Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- The ester derivative Palmitoylcarnitine abrogates cervical cancer cell survival by enhancing lipotoxicity and mitochondrial dysfunction.Cell communication and signaling : CCS · 2025Article
- Reprogramming of fatty acid metabolism: a hidden force regulating the occurrence and progression of cholangiocarcinoma.Cell death discovery · 2025Review
- CPT1A mediates succinylation of LDHA at K318 site promoteing metabolic reprogramming in NK/T-cell lymphoma nasal type.Cell biology and toxicology · 2025Article
- Protective Effect of Carvedilol Against Oxidative Stress Induced by Palmitic Acid in Primary Rat Hepatocytes.Cell biochemistry and function · 2025Article
- Mitochondrial involvement in PC: improving therapeutic strategies.Frontiers in pharmacology · 2025Review
- CPT1A mediates the succinylation of SP5 which activates transcription of PDPK1 to promote the viability and glycolysis of prostate cancer cells.Cancer biology & therapy · 2024Article
- Article
- Oxidative Stress-Associated Alteration of circRNA and Their ceRNA Network in Differentiating Neuroblasts.International journal of molecular sciences · 2024Article
- CAVPENET Peptide Inhibits Prostate Cancer Cells Proliferation and Migration through PP1γ-Dependent Inhibition of AKT Signaling.Pharmaceutics · 2024Article
- Characteristics, clinical significance, and cancer immune interactions of lipid metabolism in prostate cancer.Translational cancer research · 2024Article
- Palmitic acid induces lipid droplet accumulation and senescence in nucleus pulposus cells via ER-stress pathway.Communications biology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.