This review demonstrates metabolic impact on DNA repair in cancer cells, suggesting new therapeutic targets.
Cancer cells exhibit reprogrammed metabolic pathways to sustain aggressive phenotypes, including continuous cell division, stemness, invasion, and metastasis. Emerging evidence suggests that these metabolic adaptations profoundly impact DNA repair pathways, which contribute to the responses to therapy and influence overall outcomes. Metabolic processes such as the Warburg effect, nicotinamide adenine dinucleotide (NAD) metabolism, glutamine metabolism, and one-carbon metabolism support DNA repair by expanding the metabolite pool and facilitating post-translational modifications. Conversely, oncometabolites impair DNA repair pathways through epigenetic reprogramming, thereby promoting genomic instability. This review highlights recent discoveries that elucidate the intricate connections between metabolic hallmarks in cancer cells and DNA repair mechanisms, offering insights into potential therapeutic targets for future cancer treatments.
No takes yet. Share an insight, caveat, or question.
Chunzhang Yang (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: