m7G RNA methylation in cancer: Effect, mechanism and clinical application

RNA methylation has emerged as a pivotal layer of post-transcriptional regulation that shapes the biological behavior of cancer cells. Among the diverse chemical modifications identified-such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), 5-hydroxymethylcytosine (5hmC), and 2'-O-dimethyladenosine (m6Am)-the m7G modification has recently garnered increasing attention. Mounting evidence indicates that m7G methylation plays an essential role in RNA metabolism and profoundly influences cancer initiation and progression.

This Review synthesizes current advances in understanding the biological and clinical implications of m7G RNA methylation, with a particular focus on its key regulatory components, METTL1/WDR4 and eIF4E. We discuss how these enzymes and binding proteins orchestrate m7G deposition and recognition to modulate oncogenic processes, including cell growth, differentiation, metastasis, and therapeutic resistance. Furthermore, we highlight emerging evidence linking m7G-related pathways to broader signaling networks that govern cancer plasticity and tumor microenvironment remodeling.

m7G RNA methylation represents a rapidly evolving frontier in cancer epigenetics. The METTL1/WDR4 methyltransferase complex and eIF4E translation initiation factor have emerged as central nodes connecting RNA modification to oncogenic signaling. Targeting m7G-dependent pathways holds considerable promise for the development of novel diagnostic biomarkers and therapeutic strategies. Continued exploration of this modification may ultimately expand the landscape of RNA-based precision oncology.

m7G-driven selective regulation exerts context-dependent, two-sided effects on tumour progression. m7G modulates therapeutic response, shaping chemosensitivity and resistance. m7G holds substantial clinical promise as a diagnostic/prognostic biomarker and a therapeutic target.