Acetyl-CoA carboxylase 1 depletion suppresses de novo fatty acid synthesis and mitochondrial β-oxidation in castration-resistant prostate cancer cells.

ABSTRACT: Cancer cells, including those of prostate cancer (PCa), often hijack intrinsic cell signaling to reprogram their metabolism. Part of this reprogramming includes the activation of de novo synthesis of fatty acids that not only serve as building blocks for membrane synthesis but also as energy sources for cell proliferation. However, how de novo fatty acid synthesis contributes to PCa progression is still poorly understood. Herein, by mining public datasets, we discovered that the expression of acetyl-CoA carboxylase alpha (ACACA), which encodes acetyl-CoA carboxylase 1 (ACC1), was highly expressed in human PCa. In addition, patients with high ACACA expression had a short disease-free survival time. We also reported that depletion of ACACA reduced de novo fatty acid synthesis and PI3K/AKT si

SUBMITTER: Liu S 

PROVIDER: S-EPMC9771725 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature