METTL1-mediated internal m7G methylation of cathepsin B messenger ribonucleic acid (mRNA) promotes synovial aggression in rheumatoid arthritis
Authors' conclusion
Our findings reveal an important role of METTL1-mediated internal mRNA m7G modification in promoting synovial aggression of RA
Study context
- Population
- FLSs and synovial tissues from patients with active established rheumatoid arthritis (RA); RA animal models
Methodological detailsin vitro FLS experiments, RA animal models
- In vitro FLS experiments
- RA animal models
Main finding
As reported in the abstract
- Increased levels of METTL1 and internal mRNA m7G in FLSs and synovial tissues from patients with RA
- METTL1 knockdown or overexpression decreased or increased migration and invasion of RA FLSs
- Synovial METTL1 level positively correlated with DAS28-ESR in patients with RA
- METTL1 knockdown in vivo mitigated arthritis severity in RA animal models
- METTL1 promotes aggressive action of RA FLSs by regulating translation efficiency of internal mRNA m7G-modified cathepsin B (CTSB)
- CTSB knockdown also suppressed aggression of RA FLSs
Original publication
METTL1-mediated internal m7G methylation of cathepsin B mRNA promotes synovial aggression in rheumatoid arthritis. Ann Rheum Dis. Published 22 October 2025. doi:10.
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