Skip to main content
. 2019 Sep 20;8(10):1115. doi: 10.3390/cells8101115

Figure 8.

Figure 8

Proposed working model. In castrated conditions, increased CPT1A activity in the mitochondria increases beta-oxidation and generation of acetyl-coA. The excess of acetyl-CoA in the cytoplasm is used by the CRPC cells to acetylate histones and promote increased growth and resistance to anti-androgen therapies like enzalutamide, further promoting the castration-resistant phenotype.