ArticleOncogene2017
Deregulation of MicroRNAs mediated control of carnitine cycle in prostate cancer: molecular basis and pathophysiological consequences.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 67 citations in OpenAlex.
- Epithelial SLC25A20 Deficiency Drives Immunosuppressive Neutrophil Remodeling via ARG1 Palmitoylation to Promote Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- Fluorinated Carnitine Derivatives as Tools to Visualise Carnitine Transport and Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Novel therapeutic strategies for targeting fatty acid oxidation in cancer.Biomarker research · 2025Review
- Matairesinol Targets Lipid Metabolism Reprogramming in AR-Independent Prostate Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Comprehensive review of the expanding roles of the carnitine pool in metabolic physiology: beyond fatty acid oxidation.Journal of translational medicine · 2025Review
- MicroRNA-372-3p impairs fatty acid metabolism in hepatocellular carcinoma cells by targetingBioImpacts : BI · 2025Article
- Dysfunction of the carnitine cycle in tumor progression.Heliyon · 2024Review
- Lipid metabolism and its implications in tumor cell plasticity and drug resistance: what we learned thus far?Cancer metastasis reviews · 2024Review
- Clinical Significance of Carnitine in the Treatment of Cancer: From Traffic to the Regulation.Oxidative medicine and cellular longevity · 2023Review
- Mitochondrial CPT1A: Insights into structure, function, and basis for drug development.Frontiers in pharmacology · 2023Review
- Role of Lipids and Lipid Metabolism in Prostate Cancer Progression and the Tumor's Immune Environment.Cancers · 2022Review
- Targeting Energy Metabolism in Cancer Treatment.International journal of molecular sciences · 2022Review
- circRNA-0002109 promotes glioma malignant progression via modulating the miR-129-5P/EMP2 axis.Molecular therapy. Nucleic acids · 2022Article
- Article
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- Fatty Acid Metabolism Reprogramming in Advanced Prostate Cancer.Metabolites · 2021Review
- MiR-124-3p Suppresses Prostatic Carcinoma by Targeting PTGS2 Through the AKT/NF-κB Pathway.Molecular biotechnology · 2021Article
- Spatial differentiation of metabolism in prostate cancer tissue by MALDI-TOF MSI.Cancer & metabolism · 2021Article
- Integrative Bioinformatics Analysis Revealed Mitochondrial Defects Underlying Hypoplastic Left Heart Syndrome.International journal of general medicine · 2021Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells reprogram their metabolism to maintain both viability and uncontrolled proliferation. Although an interplay between the genetic, epigenetic and metabolic rewiring in cancer is beginning to emerge, it remains unclear how this metabolic plasticity occurs. Here, we report that in prostate cancer cells (PCCs) microRNAs (miRNAs) greatly contribute to deregulation of mitochondrial fatty acid (FA) oxidation via carnitine system modulation. We provide evidence that the downregulation of hsa-miR-124-3p, hsa-miR-129-5p and hsa-miR-378 induced an increase in both expression and activity of CPT1A, CACT and CrAT in malignant prostate cells. Moreover, the analysis of human prostate cancer and prostate control specimens confirmed the aberrant expression of miR-124-3p, miR-129-5p and miR-378 in primary tumors. Forced expression of the miRNAs mentioned above affected tumorigenic properties, such as proliferation, migration and invasion, in PC3 and LNCaP cells regardless of their hormone sensitivity. CPT1A, CACT and CrAT overexpression allow PCCs to be more prone on FA utilization than normal prostate cells, also in the presence of high pyruvate concentration. Finally, the simultaneous increase of CPT1A, CACT and CrAT is fundamental for PCCs to sustain FA oxidation in the presence of heavy lipid load on prostate cancer mitochondria. Indeed, the downregulation of only one of these proteins reduces PCCs metabolic flexibility with the accumulation of FA-intermediate metabolites in the mitochondria. Together, our data implicate carnitine cycle as a primary regulator of adaptive metabolic reprogramming in PCCs and suggest new potential druggable pathways for prevention and treatment of prostate cancer.
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