ArticleScientific reports2026
METTL3-mediated m
Article in Scientific reports, 2026. 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.
- Circular RNAs in cervical cancer: from ceRNA networks to epitranscriptomic regulation, immune modulation, and metastatic reprogramming.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
6 authors.
Funding
Abstract
Cervical cancer remains a significant global health burden. This study aimed to investigate whether the RNA methyltransferase METTL3 promotes cervical cancer progression by regulating the stability of circular RNA circCDK6 via N⁶-methyladenosine (m⁶A) modification. Clinical samples from cervical cancer patients were analyzed. In vitro and in vivo functional assays, including PCR, RNA immunoprecipitation, m⁶A-methylated RNA immunoprecipitation, RNA stability assays, CCK-8, colony formation, flow cytometry, dual-luciferase reporter assay, and xenograft models were employed using cervical cancer cell lines. METTL3 and circCDK6 were significantly upregulated in cervical cancer tissues, and high expression correlated with advanced disease and poor patient prognosis. METTL3 directly bound to circCDK6 and installed m⁶A modification, which enhanced circCDK6 RNA stability. Knockdown of METTL3 or circCDK6 suppressed cell proliferation, induced G0/G1 phase arrest, and inhibited tumor growth in mouse models. Mechanistically, circCDK6 functioned as a competitive endogenous RNA to sponge miR-449a, thereby de-repressing the expression of its target, CDK6, a key cell cycle regulator. Our findings unveil a novel oncogenic METTL3/m⁶A/circCDK6/miR-449a/CDK6 axis that promotes cervical cancer tumorigenesis, highlighting its potential as a therapeutic target for intervention.
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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.