ReviewClinical and translational medicine2025
m7G RNA methylation in cancer: Effect, mechanism and clinical application.
Review in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- N7-Methylguanosine Modification in Colorectal Cancer: Molecular Insights and Clinical Implications.International journal of molecular sciences · 2026Review
- RNA epitranscriptomic regulation of tumor immune evasion: mechanisms, context-dependent roles, and therapeutic implications.Frontiers in immunology · 2026Review
- m7G RNA methylation in cancer: Effect, mechanism and clinical application.Clinical and translational medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
backgroundRNA 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. MAIN TOPICS: 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.
conclusionsm7G 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. KEY POINTS: 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.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.