Authors : Ankit

Volume/Issue : Volume 11 - 2026, Issue 5 - May

Google Scholar : https://tinyurl.com/yf3tewu8

Scribd : https://tinyurl.com/yshhs5da

DOI : https://doi.org/10.38124/ijisrt/26May1124

Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.

Abstract : Cancer cells exhibit profound metabolic reprogramming to support uncontrolled growth, survival, and therapy resistance. In addition to a shift toward aerobic glycolysis, tumors display increased dependence on amino acids such as glutamine, serine, methionine, and cysteine, essential for biosynthesis, redox balance, and epigenetic regulation. Lipid metabolism, particularly fatty acid oxidation and lipolysis, is also upregulated, with key enzymes like ATP-citrate lyase (ACLY) and acyl-CoA synthetase short-chain family member 2 (ACSS2) facilitating acetyl-CoA production, which fuels histone acetylation and chromatin remodeling. Importantly, mitochondrial metabolism plays a pivotal role in supporting both bioenergetic and epigenetic demands, linking mitochondrial function with gene regulation. Nucleotide synthesis, both de novo and salvage, is enhanced in tumors and influenced by oncogenes and stress responses, contributing to genomic instability and metastasis. These integrated metabolic and epigenetic adaptations present promising therapeutic vulnerabilities. Targeting key metabolic enzymes and mitochondrial-epigenetic interfaces may function with gene regulation. Nucleotide synthesis, both de novo and salvage, is enhanced in tumors and influenced by oncogenes and stress responses, contributing to genomic instability and metastasis. These integrated metabolic and epigenetic adaptations present promising therapeutic vulnerabilities. Targeting key metabolic enzymes and mitochondrial-epigenetic interfaces may provide effective strategies to suppress tumor progression and overcome chemoresistant.

Keywords : Cancer Metabolism, Mitochondrial Epigenetics, Amino Acid Reprogramming, Fatty Acid Oxidation, Nucleotide Biosynthesis, Chemoresistance, Mitochondrial Epigenetics.

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