ReviewCancer cell international2025
The crosstalk of m6A modification and non-coding RNAs in gastric cancer: biomarkers and therapeutic potentials.
Review in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- HMGA2 promotes hepatocellular carcinoma progression by regulating tumor-associated macrophage via Notch1/CCL2 signaling.Molecular and cellular biochemistry · 2026Article
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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
Long non-coding RNAs (lncRNAs) are instrumental in the progression and regulation of gastric cancer (GC), affecting various cellular processes including gene expression, apoptosis, cell proliferation, and metastasis. N6-methyladenosine (m6A), a dynamic and reversible RNA modification, profoundly influences GC by modulating RNA metabolism and function, impacting RNA stability, maturation, and interactions. The crosstalk between non-coding RNAs (ncRNAs) and m6A modification is pivotal for the stability, maturation, and functional interactions of ncRNAs. Moreover, m6A-modified ncRNAs are integral in GC by regulating vital pathways involved in tumor growth and metastasis. This interaction is critical for the rapid response of cancer cells to environmental changes, facilitating their adaptation and survival. The differential expression of m6A-modified ncRNAs in GC tissues compared to normal tissues can serve as diagnostic and prognostic biomarkers, aiding in patient stratification and personalized treatment plans. Targeting m6A modification emerges as a promising therapeutic strategy for GC. Inhibiting m6A “writers” such as METTL3 can diminish the stability of oncogenic ncRNAs, thereby hindering tumor growth and metastasis. Conversely, augmenting m6A modification on tumor-suppressive ncRNAs can enhance their stability and therapeutic efficacy. This review highlights the key roles of m6A modification and ncRNAs in GC, providing valuable insights for future research and potential clinical applications.
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