Role of Metabolism and Metabolic Pathways in Prostate Cancer

Abstract

Prostate cancer (PCa) is the common cause of death in men. The pathophysiological factors contributing to PCa are not well known. PCa cells gain a protective mechanism via abnormal lipid signaling and metabolism. PCa cells modify their metabolism in response to an excessive intake of nutrients to facilitate advancement. Metabolic syndrome (MetS) is inextricably linked to the carcinogenic progression of PCa, which heightens the severity of the disease. It is hypothesized that changes in the metabolism of the mitochondria contribute to the onset of PCa. The studies of particular alterations in the progress of PCa are best accomplished by examining the metabolome of prostate tissue. Due to the inconsistent findings written initially, additional epidemiological research is required to identify whether or not MetS is an aspect of PCa. There is a correlation between several risk factors and the progression of PCa, one of which is MetS. The metabolic symbiosis between PCa cells and the tumor milieu and how this type of crosstalk may aid in the development of PCa is portrayed in this work. This review focuses on in-depth analysis and evaluation of the metabolic changes that occur within PCa, and also aims to assess the effect of metabolic abnormalities on the aggressiveness status and metabolism of PCa.

Metabolic insights into tumor pathogenesis: Unveiling pan‐cancer metabolism and the potential of untargeted metabolomics

“…When aerobic glycolysis prevents glucose from entering the TCA cycle influx, glutamine acts as the primary carbon source in the TCA cycle and FAstty acid synthesis. Myc indirectly increases FAstty acid synthesis by enhancing glutamate‐mediated TCA cycle influx through activation of GLUD 63–65 …”

“…Myc indirectly increases FAstty acid synthesis by enhancing glutamate-mediated TCA cycle influx through activation of GLUD. [63][64][65] The mevalonate pathway, which produces cholesterol, a crucial molecule for cell membrane function as well as other significant chemicals that might support tumor development and progression, is another typical lipogenic pathway that is activated in cancer. 66 Mammalian 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGCR), a rate-limiting enzyme for cholesterol biosynthesis in the mevalonate pathway, converts HMG-CoA to mevalonate.…”