{
  "abstract": "N7-methylguanosine (m7G) is distributed across several RNA classes and regulates distinct stages of gene expression. The best-characterized form is the 5′cap of messenger RNA, although m7G also occurs in transfer RNA, ribosomal RNA, internal messenger RNA, circular RNA, and transfer RNA-derived small RNAs. Cancer-associated m7G dysregulation therefore cannot be ascribed to a single enzyme or molecular outcome. The strongest causal evidence concerns the METTL1-WDR4 complex, which modifies transfer RNA and reshapes codon-biased translation, promoting proliferation, metastasis, metabolic adaptation, stress tolerance, and treatment resistance. Studies of internal messenger RNA m7G report reader-dependent effects on stability, decay, translation, and stress-granule partitioning. Cap biochemistry is established, whereas catalytic cancer mechanisms involving ribosomal RNA remain less resolved. In preclinical models, these pathways connect tumor-cell adaptation with stromal communication, immune evasion, and treatment response. The biological effects of m7G vary with the modified RNA and the proteins favored by translation; tumor-restrictive activity emerges when altered tRNA modification increases the production of cell-cycle inhibitory proteins. This review organizes established and emerging mechanisms by RNA compartment and examines the substrate-dependent balance between tumor promotion, tumor restriction, and treatment sensitivity. It also evaluates biomarker strategies, emerging pharmacological and RNA-directed interventions, and the methodological standards needed to distinguish direct m7G-dependent effects from regulator expression correlations. A site-resolved, substrate-specific understanding of m7G may reveal translational dependencies that are actionable without disrupting essential RNA metabolism in normal tissues.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": "Review",
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "name": "Xiaoxiao Tian"
    },
    {
      "name": "Di Huang"
    },
    {
      "name": "Chaonan Guan"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/bf8djk1whsdey.bib",
  "cited_by": 0,
  "doi": "10.3389/fmolb.2026.1951991",
  "fulltext_url": null,
  "id": "bf8djk1whsdey",
  "issns": [
    "2296-889X"
  ],
  "landing_url": "https://www.frontiersin.org/articles/10.3389/fmolb.2026.1951991",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "feed-journal",
      "biochemistry/general"
    ]
  ],
  "openalex": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-29",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/bf8djk1whsdey.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:16Z",
      "native_id": "10.3389/fmolb.2026.1951991",
      "source": "feed-frontiers",
      "url": "https://www.frontiersin.org/articles/10.3389/fmolb.2026.1951991"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "journal-openalex:1312|Protein Structure and Dynamics",
      "subfield": "molecular-biology"
    }
  ],
  "title": "Compartment-specific m7G RNA modification in cancer: mechanisms, tumor adaptation, and therapeutic vulnerabilities",
  "title_text": "Compartment-specific m7G RNA modification in cancer: mechanisms, tumor adaptation, and therapeutic vulnerabilities",
  "type": "peer-reviewed",
  "updated_at": "2026-10-31T00:20:30Z",
  "url": "https://research.draconitic.com/paper/bf8djk1whsdey",
  "venue": "Frontiers in Molecular Biosciences",
  "versions": []
}