ArticleInternational ophthalmology2025
METTL14-mediated m
Article in International ophthalmology, 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.
- Regulatory mechanisms and therapeutic potential of N6-methyladenosine modification in retinal diseases (Review).Molecular medicine reports · 2026Review
- Notch signaling in the tumor microenvironment: recent advances and targeted therapeutics.Molecular cancer · 2026Review
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- N6-methyladenosine: a key regulator in ocular disease mechanisms and treatment.Cell death discovery · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeRetinoblastoma (RB) is a common primary intraocular cancer developed in early childhood. The N6-methyladenosine (m
methodsThe levels of LINC00340 and methyltransferase-like 14 (METTL14) were detected using qRT-PCR. The effects of LINC00340 interacting with METTL14 on RB cells were assessed by CCK8, colony formation, and flow cytometry assays. The changes of proteins associated with Notch signaling pathway were detected using western blotting. The regulatory mechanism of LINC00340 interacting with METTL14 in RB cells was confirmed by MeRIP, qRT-PCR, and actinomycin D treatment assays.
resultsThe expression of LINC00340 and METTL14 in RB samples were elevated, as well as their levels in RB samples showed the positive correlation. Silencing LINC00340 in RB cells could impair RB cell growth and enhance apoptosis via activating Notch signaling pathway, but overexpressing LINC00340 in RB cells showed the opposite effects. In addition, upregulating METTL14 effectively relieved the repressive effects of silencing LINC00340 on RB cells due to METTL14-mediated m
conclusionsThe findings of study reveal that METTL14-mediated m
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Identifiers
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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 OpenQuestion graph.