METTL3-mediated methylation of RAC2 contributes to cell motility, oxidative stress and inflammation in TNF-α-stimulated rheumatoid arthritis fibroblast-like synovial cells.

ABSTRACT:

Background

Rheumatoid arthritis (RA) is a widely prevalent rheumatic condition causing joint inflammation and damage. RNA methylation plays an important role in RA. Herein, we intended to investigate the function of methyltransferase-like 3 (METTL3) and its N6-methyladenosine (m6A) methylation regulation for ras-related C3 botulinum toxin substrate 2 (RAC2) in RA.

Methods

MH7A cells were treated with TNF-α to establish RA cell model. The expression analysis was performed by RT-qPCR and western blot. Cellular behaviors were examined by CCK-8 assay, flow cytometry, wound healing assay and transwell assay. Oxidative stress was assessed by detecting the associated indicators. Inflammatory cytokines were measured via enzyme-linked immunosorbent assay (ELISA). Interaction between

SUBMITTER: Ren H 

PROVIDER: S-EPMC11841323 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature