ArticleScientific reports2025
YTHDF2 promotes the metastasis of oral squamous cell carcinoma through the JAK-STAT pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- YTHDF2 in inflammation: Mechanisms and therapeutic strategies.Genes & diseases · 2026Review
- The mMolecular biomedicine · 2025Review
- Total m6A RNA levels and VIRMA expression as potential diagnostic and prognostic markers in oral squamous cell carcinoma.Diagnostic pathology · 2025Article
- Novel insights into the N 6-methyladenosine modification on circRNA in cancer.Frontiers in oncology · 2025Review
- Overlapping genes connect rheumatoid arthritis and head and neck cancer: coincidence or shared immune pathophysiology?Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
RNA-binding proteins act as crucial mediators between N6-methyladenosine (m6A) modification and RNA function, playing a significant role in the recurrence and metastasis of oral squamous cell carcinoma (OSCC). YTHDF2, the first identified RNA-binding protein, has been shown to be closely associated with the prognosis of certain types of cancer. However, the role of YTHDF2 in OSCC and its underlying molecular mechanisms remain poorly understood and require further investigation. First, we analysed the expression levels of YTHDF2 and examined its correlation with clinical features using public databases and OSCC patient samples. Subsequently, a series of in vitro functional experiments were conducted to assess the effects of YTHDF2 on the proliferation, migration, and invasion capabilities of OSCC cells. Additionally, RNA-seq analysis was utilized to investigate the signalling pathways modulated by YTHDF2, which was further supported by experimental validation. Our findings revealed that YTHDF2 expression was significantly elevated in OSCC tissues and cells, with levels closely correlated with the clinical stage, pathological grade, and survival time of patients. The knockdown of YTHDF2 resulted in a significant reduction in the proliferation, migration, and invasion abilities of OSCC cells. Furthermore, RNA sequencing data indicated that silencing YTHDF2 suppressed the JAK-STAT signalling pathway, and the use of STAT3 activators reversed this suppressive effect in OSCC cells. Our study demonstrated that YTHDF2 promotes the proliferation, metastasis, and invasion of OSCC by positively regulating the JAK-STAT signalling pathway, suggesting that YTHDF2 could serve as a potential prognostic marker for the diagnosis and treatment of OSCC.
Indexed as
Identifiers
What 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.