When fat goes down, prostate cancer is on the ropes

Abstract

Reprogrammed lipid metabolism and persistent androgen receptor signaling commonly mark aggressive prostate cancer. We describe that targeting de-novo lipogenesis deprives prostate cancer cells of substrates and fuel, while inhibiting androgen receptor signaling. Our study uncovers the interplay between lipogenesis and androgen receptor and proposes novel combinatorial therapeutic approaches.

Keywords

• metastatic prostate cancer
• fatty acid synthesis
• androgen receptor
• lipid metabolism
• reticulum endoplasmic stress response