ArticleCellular oncology (Dordrecht, Netherlands)2025
METTL1-WDR4 promotes the migration and proliferation of gastric cancer through N
Article in Cellular oncology (Dordrecht, Netherlands), 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
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
2 citing papers in PubMed.
- METTL1/WDR4 Complex: A Novel Epitranscriptomic Target at the Crossroads of RNA Methylation and Drug Discovery.Journal of medicinal chemistry · 2026Review
- The emerging roles of METTL1-mediated tRNA mFrontiers in immunology · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer (GC) is one of the most common malignant tumor worldwide. Metastasis is leading cases of cancer-related death of GC. It has been found that N
methodsRT-qPCR, WB and IHC were used to detect the expression of METTL1 and WDR4 in GC cells and tissues. Function-based experiments were performed using METTL1-WDR4 knockdown and overexpression cell lines in vitro and in vivo, including CCK8, colony formation, transwell and nude mice models. Mechanistically, RNA-seq, MeRIP-seq, MeRIP-qPCR, western blot, dot blot, co-IP, ChIP and IHC stainings were performed.
resultsMETTL1 and WDR4 were upregulated in GC patients. High expression of METTL1 and WDR4 were associated with poor prognosis. Silencing METTL1-WDR4 inhibited GC cell migration and proliferation in vitro and vivo. Mechanistically, METTL1-WDR4 can enhance the mRNA stability of PIK3C2B and AKT by promoting their m7G levels, which leading the overexpression of p-AKT. Interestingly, we also found that on the one hand, the transcription factor YY1 can promote the mRNA transcription expression of METTL1 and WDR4 at the same time, and on the other hand, METTL1-WDR4 can promote YY1 expression by increasing the level of m7G. This regulation presents positive feedback. Above all, METTL1 and WDR4 ultimately up-regulate the level of m7G and promote the malignant progression of GC.
conclusionsThese findings suggest that METTL1-WDR4 might serve as a potential diagnostic and prognostic biomarker and a therapeutic target for GC treatment by regulating m7G level.
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.