ArticleOdontology2025
COL1A1, mediated by m6A methylation of METTL3, facilitates oral squamous cell carcinoma cell growth and metastasis.
Article in Odontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Article
- N6-methyladenosine RNA modification in head and neck squamous cell carcinoma (HNSCC): current status and future insights.Medical oncology (Northwood, London, England) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen type I alpha1 (COL1A1) has been found to be abnormal expressed in oral squamous cell carcinoma (OSCC) tissues, but its role and mechanism in OSCC need to be further elucidated. The expression levels of COL1A1 and methyltransferase-like 3 (METTL3) were measured by quantitative real-time PCR and western blot. Cell growth and metastasis were determined by CCK8, colony formation, EdU, flow cytometry and transwell assays. MeRIP, Co-IP and dual-luciferase reporter assays were performed to explore the interplay of COL1A1 and METTL3. COL1A1 mRNA stability was confirmed by Actinomycin D assay. Mice xenograft models were constructed to perform in vivo experiments. COL1A1 and METTL3 were upregulated in OSCC. COL1A1 knockdown suppressed OSCC cell growth and metastasis, while its overexpression had an opposite effect. The stability of COL1A1 mRNA was regulated by the m6A methylation of METTL3. METTL3 overexpression promoted OSCC cell growth and metastasis, and its knockdown-mediated OSCC cell function inhibition could be abolished by COL1A1 overexpression. Besides, silencing of METTL3 reduced OSCC tumor growth by reducing COL1A1 expression. METTL3-stabilized COL1A1 promoted OSCC progression, providing an exact molecular target for the treatment of OSCC.
Indexed as
Identifiers
38900231What Socratic 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 Socratic graph.