ArticleCancer & metabolism2024
The polyunsaturated fatty acid docosahexaenoic affects mitochondrial function in prostate cancer cells.
Article in Cancer & metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Docosahexaenoic Acid Enhances the Cytotoxic Effects of Enzalutamide and the PARP Inhibitor in Castration-Resistant Prostate Cancer Cell Lines.International journal of molecular sciences · 2026Article
- The omega-3 DHA induces pyroptosis and mitochondrial dysfunction in ovarian cancer cells via ROS and caspase-1 activation.Cell death discovery · 2026Article
- Linolenic Acid Inhibits Cancer Stemness and Induces Apoptosis by Regulating Nrf2 Expression in Gastric Cancer Cells.Current issues in molecular biology · 2025Article
- Effects of Docosahexaenoic Acid on Prostate Cancer.Journal of xenobiotics · 2025Review
- Review
- DHA suppresses hormone-sensitive and castration-resistant prostate cancer growth by decreasing de novo lipogenesis.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2025Article
- Distinct proteomic profiles of plasma-derived extracellular vesicles in healthy, benign, and triple-negative breast cancer: candidate biomarkers for liquid biopsy.Scientific reports · 2025Article
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9 authors.
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Abstract
backgroundProstate cancer (PCa) shows a rewired metabolism featuring increased fatty acid uptake and synthesis via de novo lipogenesis, both sharply related to mitochondrial physiology. The docosahexaenoic acid (DHA) is an omega-3 polyunsaturated fatty acid (PUFA) that exerts its antitumoral properties via different mechanisms, but its specific action on mitochondria in PCa is not clear. Therefore, we investigated whether the DHA modulates mitochondrial function in PCa cell lines.
methodsHere, we evaluated mitochondrial function of non-malignant PNT1A and the castration-resistant (CRPC) prostate 22Rv1 and PC3 cell lines in response to DHA incubation. For this purpose, we used Seahorse extracellular flux assay to assess mitochondria function, [
resultsIn all cell lines DHA decreased basal respiratory activity, ATP production, and the spare capacity in mitochondria. Also, the omega-3 induced mitochondrial hyperpolarization, ROS overproduction and changes in membrane phosphatidylglycerol composition. In PNT1A, DHA led to mitochondrial fragmentation and it increased glycolysis while in cancer cells it stimulated glucose oxidation, but decreased de novo lipogenesis specifically in 22Rv1, indicating a metabolic shift. In all cell lines, DHA modulated several metabolites related to energy metabolism and it was incorporated in phosphatidylglycerol, a precursor of cardiolipin, increasing the unsaturation index in the mitochondrial membrane. Accordingly, DHA triggered cell death mainly in PNT1A and 22Rv1.
conclusionIn conclusion, mitochondrial metabolism is significantly affected by the PUFA supplementation to the point that cells are not able to proliferate or survive under DHA-enriched condition. Moreover, combination of DHA supplementation with inhibition of metabolism-related pathways, such as de novo lipogenesis, may be synergistic in castration-resistant prostate cancer.
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