Glutamine metabolism serves as a metabolic intersection in prostate cancer ammonium reprogramming, where this conditionally essential amino acid propels tumor proliferation through multifaceted biosynthetic and bioenergetic contributions including its catabolic flux furnishes precursors for de novo purine/pyrimidine biosynthesis and hexosamine pathway activation, drives reductive carboxylation-dependent lipogenesis, sustains redox homeostasis via glutathione synthesis and NADPH regeneration, generates non-essential amino acids, and fuels mitochondrial oxidative phosphorylation through -KG (-ketoglutarate) mediated anaplerosis, collectively establishing glutaminolysis as an indispensable axis supporting prostate cancer malignancy ( MYC functions as a central regulator of glutamine metabolism in prostate cancer by repressing miR-23a/b, thereby relieving the inhibition of mitochondrial GLS and promoting glutaminolysis, particularly in androgen-independent PC-3 cells ( Metabolomic profiling reveals elevated alanine levels in PCa versus normal prostate tissues, potentially reflecting heightened membrane biosynthesis requirements (56)
L., Nakeeb A., Pitt H
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H., Harken, A
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