ArticleCancer medicine2025
The Oncogenic Role of UBXN1 in Gastric Cancer Is Attributed to the METTL16-Mediated m6A Methylation and Histone Modifications.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- RNA modification-mediated multidimensional crosstalk: a novel perspective on gene expression regulation.Genome biology · 2026Review
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- Metabolic reprogramming-associated genomic instability drives colorectal cancer progression via the UBXN1-NF-κB axis.American journal of translational research · 2026Article
- IL-23 promotes PD-L1 expression and tumor immune evasion via METTL16 pathway.American journal of cancer research · 2026Article
- METTL16 emerges as a pivotal epitranscriptomic regulator, linking RNA modification, tumor progression, and immune modulation.Frontiers 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
7 authors.
Funding
Abstract
backgroundMultiple epigenetic regulatory mechanisms are crucial in tumorigenesis and development. However, the synergistic relationship between N6-methyladenosine (m6A) and histone modifications in regulating gene expression of gastric cancer (GC) requires further investigation.
resultsHere, based on the microarray, RNA-seq, and survival analysis data, the m6A methyltransferase METTL16 was identified as a potential tumorigenic factor of GC. The silence of METTL16 suppresses the malignant phenotype of GC cells, and the NF-κB pathway was activated. By using the weighted correlation network analysis (WGCNA) and integrating RNA-seq and MeRIP-seq data, it was found that METTL16 is significantly positively correlated with UBX domain protein 1 (UBXN1). Furthermore, through the MeRIP-qPCR and dual-luciferase reporter assays, we found that knocking down METTL16 reduced the m6A modification level of the UBXN1 coding sequence in GC. Interestingly, the silencing of METTL16 also downregulated UBXN1 expression by promoting H3K36me3 modification at the UBXN1 promoter. Subsequent investigations found that the silencing of METTL16 upregulated the expression of the major H3K36me3 methyltransferase SETD2 in GC cells by methylating the m6A site in the mRNA coding sequence of SETD2.
conclusionsOur findings demonstrate the spatio-temporal regulation of UBXN1 expression in GC cells by METTL16 through a combination of transcriptional and post-transcriptional mechanisms. The synergistic interplay of these various epigenetic mechanisms provides new prospects for tumor diagnosis and precision treatment.
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.