ArticleClinical and experimental medicine2024
FUS and METTL3 collaborate to regulate RNA maturation, preventing unfolded protein response and promoting gastric cancer progression.
Article in Clinical and experimental medicine, 2024. 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.
- NEAT1: a multifaceted long non-coding RNA in multiple myeloma.Haematologica · 2026Review
- CircLRIG1 inhibits the malignant phenotypes of colorectal cancer cells by inactivating the NF-κB signaling through interaction with FUS.Discover oncology · 2026Article
- Defining the RNA Modification Landscape of Multiple Myeloma Reveals METTL3-Dependent mbioRxiv : the preprint server for biology · 2026Article
- FOXM1/FUS facilitates triple-negative breast cancer malignant progression and glutamine metabolism through mediating SLC7A5 transcription.Journal of molecular histology · 2026Article
- Cell-Free DNA Methylation-Based Liquid Biopsy Assay to Identify Lymph Node Metastasis in T1 Gastric Cancer.United European gastroenterology journal · 2025Article
- TRIM32 promotes tumor immune evasion and impedes Anti-PD-1 treatment by inducing immunosuppressive macrophages in gastric cancer.Journal of translational 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
4 authors.
Funding
Abstract
FUS-mediated alternative splicing and METTL3-regulated RNA methylation play crucial roles in RNA processing. The purpose of this study was to investigate the interactive roles of FUS and METTL3 in gastric cancer (GC) progression. RNA sequencing data were obtained from the TCGA-STAD dataset. Differentially expressed genes (DEGs) were analyzed across groups stratified by the medians of FUS, METTL3, and NEAT1, respectively. Endoplasmic reticulum (ER) stress markers PERK, IRE1, pIRE1, Bip, and CHOP, as well as related apoptosis stress markers PARP, cleaved-PARP, (Cleaved) Caspase 7, and (Cleaved) Caspase 3, were assessed through western blotting. Alternative splicing and N6-methyladenosine (m(6)A) methylation of specific genes were detected with MeRIP-PCR. Finally, in vivo experiments were conducted using nude mice bearing sh-FUS-transfected HGC27 xenograft tumors. FUS and METTL3 expression levels were elevated in GC tissues. A significant overlap of DEGs was observed between the FUS- and METTL3-stratified groups. These overlapping DEGs were predominantly enriched in mRNA processing and protein processing in the ER. ER stress and apoptosis were induced by sh-FUS or sh-METTL3, which was further enhanced by ER stress inducer tunicamycin in both MKN45 and HGC27 cells. Similarly, DEGs for NEAT1 high- and low-expressed groups were enriched in protein processing in the ER and spliceosome. To a lesser extent, ER stress was also induced by sh-NEAT1 and enhanced by tunicamycin in HGC27 cells. Furthermore, sh-FUS or sh-METTL3 influenced alternative splicing and methylation of specific mRNAs, including FUS, NEAT1, PCNA, MCM2, and BIRC5. Tumor progression was inhibited by sh-FUS in mice, and ER stress and apoptosis were induced, which were further enhanced by tunicamycin. FUS and METTL3 collaborate to facilitate RNA maturation. Inhibiting FUS or METTL3 promoted ER stress and apoptosis and inhibited progression in GC.
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.