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Peroxisomal branched chain fatty acid ?-oxidation pathway is upregulated in prostate cancer

2004; Wiley; Volume: 63; Issue: 4 Linguagem: Inglês

10.1002/pros.20177

1097-0045

Shan Zha, Sacha Ferdinandusse, Jessica Hicks, Simone Denis, Thomas A. Dunn, Ronald J. A. Wanders, Jun Luo, Angelo M. De Marzo, William B. Isaacs,

Cancer, Lipids, and Metabolism

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. © 2004 Wiley-Liss, Inc.