FIGURE 2.

How metabolic alterations impact nuclear gene regulation in cancer. Abnormal metabolic activities in tumor cells facilitate alterations in chromatin or protein modifications such as methylation (Met), acetylation (Ac), O‐glycosylation (G), and lipidation (L), mediated through the control of key metabolites like SAM, acetyl‐CoA, UDP‐GlcNAc, and lipids. Nuclear metabolic enzymes, originating from specific metabolic pathways, exert their influence on chromatin architecture, DNA repair mechanisms, and gene transcription through diverse regulatory avenues. Perturbations in epigenomic stability or genomic fidelity can reciprocally affect the transcriptional profile of metabolic genes, thus establishing a dynamic metabolism‐epigenetics nexus that enables tumor cells to adapt and thrive in variable environments.