TL;DR
This narrative review examines how alterations in fatty acid oxidation, lipid uptake, cholesterol metabolism and lipid-derived metabolites converge on the sirtuin family of NAD+-dependent enzymes to regulate epigenetic states in cancer.
Lipid metabolism is no longer viewed simply as a source of membrane biomass or ATP. It is now proposed as a regulatory system that determines which metabolites reach the nucleus, which chromatin-modifying enzymes are engaged, and which transcriptional states become stable during disease progression. This review develop...
Cancer cells undergo extensive metabolic reprogramming to sustain rapid proliferation and adapt to heterogeneous tumour microenvironments. These metabolic alterations are tightly linked to epigenetic regulation, which reshapes gene expression and cellular signalling mechanisms. Among epigenetic regulators, histone deac...
Histone methylation regulates chromatin structure and gene expression, whereas tumor metabolism provides bioenergetic and biosynthetic inputs. These processes are bidirectionally linked: S-adenosylmethionine supplies methyl groups for histone methyltransferases, α-ketoglutarate(α-KG) supports JmjC-domain demethylases,...
This review comprehensively summarizes the multifaceted roles of major histone modifications, including acetylation, methylation, ubiquitination, phosphorylation, and emerging metabolism-linked acylations, in governing critical DNA-templated processes such as replication, transcription, and the DNA damage response.
Protein lysine acetylation is a widespread post-translational modification that regulates metabolic enzyme activity and cellular function. Sirtuins (SIRTs) are a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases that act as key metabolic sensors coupling cellular energy status to the regulation...
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