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We are analyzing https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-025-02334-8.

Title:
METTL14 modulates the progression and ferroptosis of colitis by regulating the stability of m6A-modified GPX4 | European Journal of Medical Research | Full Text
Description:
Ulcerative colitis (UC) is non-specific inflammatory bowel disease. UC development and progression were closely associated with epigenetic modifications. Nevertheless, the specific relationship between N6-methyladenosine (m6A) modification at RNA transcription levels and UC pathogenesis remains unclear. We established UC cell models and mouse models through dextran sulfate sodium (DSS) induction. The expression levels of METTL14 were analyzed via qRT-PCR and western blot. In vitro functional experiments evaluated the effects of METTL14 overexpression on the viability of DSS-induced NCM460 cells and ferroptosis markers. Use of the m6A methylation detection kit, MeRIP-qPCR, and RNA stability experiments confirmed the molecular mechanism controlled by METTL14. In vivo experiments with inflammatory mice models elucidated the interaction between METTL14 and GPX4. Findings from this study indicated a notable reduction in m6A methyltransferase METTL14 expression in DSS-induced NCM460 cells and DSS-induced mice models. METTL14 overexpression effectively suppressed ferroptosis in DSS-induced NCM460 cells. In addition, METTL14 enhanced GPX4 mRNA stability through mediating m6A modification, and the interplay between METTL14 and GPX4 through m6A modification introduced innovative therapeutic approaches for UC management.
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Keywords {🔍}

mettl, cells, pubmed, gpx, cell, article, google, scholar, ferroptosis, ncm, mice, dss, expression, colitis, levels, cas, fig, modification, mrna, inflammatory, group, rna, intestinal, central, iron, gsh, dssinduced, oemettl, groups, progression, colon, treatment, mda, overexpression, study, model, research, stability, disease, experiments, dai, ros, score, chen, ulcerative, cancer, inflammation, subsequently, protein, assessed,

Topics {✒️}

regulating ampk/mtor/p70s6k-mediated autophagy mettl3-mediated pre-mir-34a sds-page gel electrophoresis galectin-3/tlr4/nf-κb pathway exosomal mir-34a-5p residual dcfh-da dye mettl3/alkbh5/ythdf2 regulated dss + oe-mettl14 + sh-gpx4 dss + oe-mettl14 + sh-nc springer nature sh-gpx4 significantly countered copper-dependent autophagic degradation sh-gpx4 partially counteracting mettl14-mediated m6a modification nrf2-gpx4 signaling pathway additional information publisher' ferroptosis-induced cell death dss-treated ncm460 cells dss-induced ncm460 cells m6a methylation-related genes iron death-related markers aforementioned dss-treated cells oe-mettl14 + sh-gpx4 author ying zhou oe-mettl14 + sh-nc ythdf1-traf6 pathway regulates privacy choices/manage cookies sh-gpx4 partly mitigated alleviates experimental colitis dss-induced mice models dextran sulfate sodium alleviate chemotherapy responsiveness n6-methyladenosine modification participates mediated m6a modification inflammatory bowel disease bmc inflammatory cytokines tnf-α intestinal mucosal inflammation induced experimental colitis authors scientific editing dss-induced uc mice intestinal epithelial barrier account european journal epithelial injury score fresh colon tissue references yang normal group received merip-qpcr merip-qpcr mucosal muscular infiltration = 2 dss-induced colitis

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What does disease progression look like in ulcerative colitis, and how might it be prevented?

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