Lipid Metabolic Reprogramming During Progression to Castration-resistant Prostate Cancer Identified by Quantitative Proteomics.
1/5 보강
[BACKGROUND/AIM] The progression of hormone-sensitive prostate cancer (HSPC) to castration-resistant prostate cancer (CRPC) as a result of resistance to androgen deprivation therapy (ADT) remains a ma
APA
Sim H, Bae S, et al. (2025). Lipid Metabolic Reprogramming During Progression to Castration-resistant Prostate Cancer Identified by Quantitative Proteomics.. Cancer genomics & proteomics, 22(6), 940-952. https://doi.org/10.21873/cgp.20548
MLA
Sim H, et al.. "Lipid Metabolic Reprogramming During Progression to Castration-resistant Prostate Cancer Identified by Quantitative Proteomics.." Cancer genomics & proteomics, vol. 22, no. 6, 2025, pp. 940-952.
PMID
41151856 ↗
Abstract 한글 요약
[BACKGROUND/AIM] The progression of hormone-sensitive prostate cancer (HSPC) to castration-resistant prostate cancer (CRPC) as a result of resistance to androgen deprivation therapy (ADT) remains a major challenge in prostate cancer treatment.
[MATERIALS AND METHODS] To explore the underlying mechanisms, we performed deep comparative proteomic profiling of HSPC and CRPC cell lines. LNCaP and C4-2 cell lines were cultured in isotopically labeled medium, combined, and digested, followed by liquid chromatography-mass spectrometry (LC-MS/MS) and bioinformatic analyses.
[RESULTS] Using SILAC-based proteomic analysis, 3,578 proteins were identified, with 2,474 quantified. In C4-2 cells, 41 proteins were significantly up-regulated, while 201 were down-regulated (fold-change >1.5 or <1.5-1, <0.05). KEGG pathway analysis linked the increased proteins to fatty acid metabolism and biosynthesis of unsaturated fatty acids. Lipidomic analysis showed a significant rise in fatty acids like DHA, palmitic acid, stearic acid, and arachidic acid, aligning with the proteomic findings.
[CONCLUSION] These results suggest that fatty acids play a key role in HSPC's progression to CRPC, possibly indicating that CRPC cells themselves may generate fatty acids.
[MATERIALS AND METHODS] To explore the underlying mechanisms, we performed deep comparative proteomic profiling of HSPC and CRPC cell lines. LNCaP and C4-2 cell lines were cultured in isotopically labeled medium, combined, and digested, followed by liquid chromatography-mass spectrometry (LC-MS/MS) and bioinformatic analyses.
[RESULTS] Using SILAC-based proteomic analysis, 3,578 proteins were identified, with 2,474 quantified. In C4-2 cells, 41 proteins were significantly up-regulated, while 201 were down-regulated (fold-change >1.5 or <1.5-1, <0.05). KEGG pathway analysis linked the increased proteins to fatty acid metabolism and biosynthesis of unsaturated fatty acids. Lipidomic analysis showed a significant rise in fatty acids like DHA, palmitic acid, stearic acid, and arachidic acid, aligning with the proteomic findings.
[CONCLUSION] These results suggest that fatty acids play a key role in HSPC's progression to CRPC, possibly indicating that CRPC cells themselves may generate fatty acids.
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