Crosstalk between m6A modification and metabolic reprogramming in colorectal cancer: from the immune microenvironment to clinical applications
TL;DR
The molecular mechanisms through which m6A modification drives the malignant progression of CRC via metabolic regulation are reviewed, the metabolic network involving m6A modification and its role in shaping TME is elucidated, and the clinical potential of targeting m6A modification and/or metabolic pathways is discussed.
Abstract
N6-methyladenosine (m6A) modification is the most common epigenetic alteration in eukaryotic mRNA, significantly impacting metabolic reprogramming and the tumor microenvironment (TME) of colorectal cancer (CRC) by dynamically regulating RNA metabolic processes. Recent studies indicate that m6A modification interacts with CRC metabolic reprogramming, fostering an immunosuppressive TME. Specifically, m6A modification promotes CRC progression by regulating glucose, lipid, and amino acid metabolism while inhibiting the activity of antitumor immune cells (such as T cells, natural killer cells, and macrophages) and activating tumor immunosuppressive cells (including tumor-associated macrophages, myeloid-derived suppressor cells, regulatory T cells, tumor-associated neutrophils, and cancer-associated fibroblasts). This article systematically reviews the molecular mechanisms through which m6A modification drives the malignant progression of CRC via metabolic regulation, elucidates the metabolic network involving m6A modification and its role in shaping TME, and discusses the clinical potential of targeting m6A modification and/or metabolic pathways, offering novel research avenues for CRC treatment.