ReviewMolecular biology reports2025
METTL3 in colorectal cancer: molecular insights and clinical implications.
Review in Molecular biology reports, 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.
- Methyltransferase 3 promotes v-set and transmembrane domain-containing 2-like protein expression to intensify ferroptosis-mediated prostate adenocarcinoma progression through the m6A methylation modification.Histology and histopathology · 2026Article
- Regulatory mechanisms and therapeutic potential of N6-methyladenosine modification in retinal diseases (Review).Molecular medicine reports · 2026Review
- mRNA processing in cancer immunotherapy: emerging targets, resistance mechanisms, and therapeutic opportunities.Frontiers in immunology · 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methyltransferase-like protein 3 (METTL3) functions as the primary "writer" of N6-methyladenosine (m6A), the most prevalent internal mRNA modification in eukaryotes. Functionally, METTL3 regulates a broad spectrum of cellular processes, including cell cycle progression, proliferation, apoptosis, invasion, migration, and differentiation. In colorectal cancer, METTL3 expression is frequently upregulated and has been correlated with poor prognosis. Therefore, this review attempts to organize and describe the main molecular and cellular mechanisms through which METTL3 drives colorectal cancer. Mechanistically, METTL3 contributes to tumor growth, metastatic dissemination, and the development of resistance to chemotherapy and radiotherapy. Special emphasis is placed on the clinical relevance of METTL3, not only as a biomarker, but also as a potential therapeutic target. Less explored topics are also addressed, such as the interaction between METTL3 and gut microbiota. Altogether, this review underscores the multifaceted role of METTL3 in colorectal cancer and the importance of further investigation to translate these insights into clinical applications.
Indexed as
Identifiers
41258268What 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.