Table 2 Putative oncometabolites defined by metabolomics.
Oncometabolite | Primary role | Key findings | Epigenetic impact | Therapeutic implications | References |
|---|---|---|---|---|---|
Sarcosine | One-carbon metabolism | Associated with prostate cancer progression | Elevates SAM; promotes CpG island methylation in prostate cells | Limited diagnostic utility; potential as an epigenetic modifier | |
Glycine | Serine–glycine one-carbon pathway | Supports purine biosynthesis, DNA methylation and tumor growth; GLDC drives metabolic reprogramming | Provides one-carbon units for SAM synthesis; links metabolism to epigenetic regulation | Targeting GLDC may inhibit tumor initiation; promising in non-small-cell lung cancer | |
Hypotaurine | Cysteine metabolism | Elevated in GBM; promotes tumor grade progression; inhibits HIF-1α hydroxylation | Unexplored but may influence hypoxia-induced epigenetic changes | ADO inhibition reduces tumor growth | |
Kynurenine | Tryptophan metabolism | Enhances NAD+ synthesis, promotes AHR signaling, supports energy metabolism and DNA repair | Affects histone deacetylation via NAD+-dependent sirtuins; potential chromatin-remodeling effects | Targeting tryptophan metabolism and kynurenine pathways may modulate tumor metabolism | |
MGO | Glycolysis byproduct | Drives protein glycation; promotes cell cycle progression and YAP activation in breast cancer | Modifies histones, disrupting chromatin structure and DNA repair | Glyoxalase 1 inhibition; potential for targeting AGE-related pathways |