Abstract
Overexpression of α-methylacyl-CoA racemase (AMACR), an enzyme involved in branched chain fatty acid β-oxidation, in prostate cancer has been reported. Here, we report that an enzyme downstream from AMACR in the peroxisomal branched chain fatty acid β-oxidation pathway - D-bifunctional protein (DBP) - is also upregulated in prostate cancer at both mRNA and protein levels, accompanied by increased enzymatic activity. Furthermore, our data suggest that pristanoyl-CoA oxidase (ACOX3), which is expressed at extremely low level in other human organs studied including the liver, might contribute significantly to peroxisomal branched chain fatty acid β-oxidation in human prostate tissue and some prostate cancer cell lines. In contrast to these results for peroxisomal enzymes, no significant expression changes of mitochondrial fatty acid β-oxidation enzymes were observed in prostate cancer tissues through comprehensive quantitative RT-PCR screening. These data for the first time provide evidence for the selective over-activation of peroxisomal branched chain fatty acid β-oxidation in prostate cancer, emphasizing a new metabolic change during prostate oncogenesis.
Original language | English (US) |
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Pages (from-to) | 316-323 |
Number of pages | 8 |
Journal | Prostate |
Volume | 63 |
Issue number | 4 |
DOIs | |
State | Published - Jun 1 2005 |
Keywords
- Acyl-CoA oxidase
- D-bifunctional protein
- Peroxisome
- Prostate cancer
- β-oxidation
ASJC Scopus subject areas
- Oncology
- Urology