Metabolic Regulation of the Epitranscriptome

Area of Science:

• Cancer Biology
• Metabolic Regulation
• Gene Expression

Background:

• Emerging evidence links cellular metabolism to oncogenic gene expression.
• Metabolic enzymes utilize cofactors crucial for gene regulation, such as acetyl-CoA, S-adenosylmethionine, and 2-ketoglutarate.
• Metabolism influences gene regulation via epigenetic and epitranscriptomic modifications.

Purpose of the Study:

• To review recent studies on metabolic regulation of the epitranscriptome.
• To explore mechanisms by which metabolism impacts RNA post-transcriptional modifications.
• To compare metabolic regulation of the epigenome and epitranscriptome.

Main Methods:

• Literature review of studies investigating metabolic regulation of epitranscriptomic enzymes.
• Analysis of mechanisms including cofactor inhibition, cofactor depletion, and writer localization.
• Comparative analysis of metabolic control over epigenome and epitranscriptome.

Main Results:

• Metabolism regulates epitranscriptomic writers and erasers (FTO, TET2, NAT10, MTO1, METTL16).
• Three key mechanisms mediate metabolic impact: cofactor inhibition, cofactor depletion, and writer localization.
• Similarities and differences exist between metabolic regulation of the epigenome and epitranscriptome.

Conclusions:

• Metabolic dysregulation directly influences oncogenic gene expression through the epitranscriptome.
• Understanding these metabolic links offers new avenues for cancer research and therapeutic strategies.
• Further investigation is needed to fully elucidate the interplay between metabolism, epitranscriptome, and cancer.