Metabolic reprogramming is a hallmark of
malignancy. It implements profound metabolic changes to sustain
cancer cell survival and proliferation. Although the Warburg effect is a common feature of metabolic reprogramming, recent studies have revealed that
tumor cells also depend on mitochondrial metabolism. Due to the essential role of mitochondria in metabolism and cell survival, targeting mitochondria in
cancer cells is an attractive therapeutic strategy. However, the metabolic flexibility of
cancer cells may enable the upregulation of compensatory pathways, such as glycolysis, to support
cancer cell survival when mitochondrial metabolism is inhibited. Thus, compounds capable of targeting both mitochondrial metabolism and glycolysis may help overcome such resistance mechanisms. Normal prostate epithelial cells have a distinct metabolism as they use
glucose to sustain physiological
citrate secretion. During the transformation process,
prostate cancer cells consume
citrate to mainly power oxidative phosphorylation and fuel lipogenesis. A growing number of studies have assessed the impact of
triterpenoids on
prostate cancer metabolism, underlining their ability to hit different metabolic targets. In this review, we critically assess the metabolic transformations occurring in
prostate cancer cells. We will then address the opportunities and challenges in using
triterpenoids as modulators of
prostate cancer cell metabolism.