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Peroxisomal 2,4-dienoyl-CoA reductase 2 (DECR2) is a short-chain dehydrogenase/reductase enzyme located in peroxisomes, responsible for the auxiliary step in the β-oxidation of unsaturated fatty acids by reducing 2,4-dienoyl-CoA intermediates to trans-3-enoyl-CoA[4][6]. This activity is critical for the efficient lipid metabolism in cells. In cancer, especially advanced and castrate-resistant prostate cancer, DECR2 is upregulated and contributes to cell cycle progression, cell proliferation, and migration by regulating lipid metabolic pathways. DECR2 is considered a promising therapeutic target in cancer due to its role in driving treatment resistance and supporting tumor growth, with ongoing research efforts exploring pharmacological inhibition as a strategy to suppress tumor viability and overcome therapy resistance[1][2][5][6].
Inhibition of DECR2 disrupts peroxisomal fatty acid oxidation, leading to decreased cell proliferation and induction of cell cycle arrest in treated cancer cells Co-inhibition of peroxisomal and androgen receptor pathways enhances tumor suppression in prostate cancer models
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