ArticleJournal of translational medicine2026
METTL3-mediated m
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Adaptation of Non-Invasive Cancer Cells to 3D Collagen I Microenvironment Induces Transcriptional Reprogramming Accompanied by a More Complex RNA Landscape.International journal of molecular sciences · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundColorectal cancer (CRC), a prevalent malignancy of the digestive system, is often characterized by poor patient prognosis due to high rates of recurrence and metastasis. N6-methyladenosine (m
methodsWe first integrated bioinformatic analysis data, which revealed a significant positive correlation and co-enrichment of methyltransferase-Like 3 (METTL3) and the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in a high-risk prognostic signature. Functional validation included in vitro assessments of cellular proliferation, migration, invasion, apoptosis, and m
resultsMETTL3 and MALAT1 were markedly upregulated in CRC tissues and cell lines. Molecular docking identified trihydroxy methylcyclohexane aminoglycoside (TMA) as a high-affinity METTL3-binding compound. Inhibition of METTL3 or MALAT1 significantly impaired cellular proliferation, migration, and invasion, while promoting apoptosis. RNA immunoprecipitation quantitative PCR (RIP-qPCR) and RNA stability assays established that METTL3 maintains MALAT1 stability via m
conclusionsCollectively, our work elucidates the METTL3-m
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Registered trials
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