ReviewCell biology and toxicology2025
METTL3-driven m⁶A epigenetics in gastric cancer: unveiling oncogenic networks and clinical translation from tumorigenesis to therapy resistance.
Review in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed.
- Ubiquitination and NOncology letters · 2026Review
- Regulatory mechanisms and therapeutic potential of N6-methyladenosine modification in retinal diseases (Review).Molecular medicine reports · 2026Review
- Integrated multi-omics analysis reveals tumor-suppressive phenotypes and associated transcriptomic remodeling upon METTL3 overexpression in A549 lung cancer cells.Translational cancer research · 2026Article
- The role of m6A RNA methyltransferase METTL3 in drug resistance mechanisms in acute myeloid leukemia.Blood research · 2026Review
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
No grant is acknowledged in the PubMed record.
Abstract
Globally, gastric cancer (GC) ranks among the deadliest malignancies due to frequent late-stage detection, metastatic dissemination, and resistance to therapies. Emerging evidence highlights N⁶-methyladenosine (m⁶A) modification, orchestrated by methyltransferase-like 3 (METTL3), as a pivotal epigenetic driver of GC pathogenesis. While METTL3 is implicated in promoting tumorigenesis, metastasis, and chemoresistance, a systematic synthesis of its multi-layered regulatory networks and clinical relevance remains elusive. This review comprehensively deciphers METTL3's dual roles as an oncogene and RNA modifier, elucidating its mechanisms in reprogramming GC progression through m⁶A-dependent RNA stability, translation, and non-coding RNA interactions. We reveal novel axes such as HOXA10-TGFβ /Smad-METTL3, METTL3/IGF2BP3-HDGF-glycolysis, and METTL3-YTHDF1- PARP1-driven chemoresistance, underscoring its cross-talk with oncogenic signaling and metabolic reprogramming. Crucially, we pioneer a clinical perspective by evaluating METTL3's diagnostic potential as a biomarker and its therapeutic vulnerability in immunotherapy and NSAID-based strategies. Our analysis identifies METTL3 as a central node in GC's molecular landscape, bridging epigenetic dysregulation with malignant phenotypes and therapy failure. These insights not only redefine METTL3's role in GC but also provide a roadmap for targeting m⁶A machinery in precision oncology.
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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 Socratic graph.