METTL3-mediated m6A modification of lncRNA MALAT1 promotes colorectal cancer progression by activating the NF-κB signaling pathway

BACKGROUND: A modification in CRC pathogenesis remain incompletely understood. METHODS: A modification levels. Finally, mechanistic profiling was conducted to dissect NF-κB pathway activity. RESULTS: A modification. In vivo, suppression of METTL3 potently inhibited xenograft tumor growth without observable toxicity. Western blot and immunohistochemistry (IHC) analyses further verified that this METTL3-MALAT1 axis activates the NF-κB pathway by modulating IκBα degradation and p65 nuclear translocation. CONCLUSIONS: A-MALAT1-NF-κB regulatory axis in CRC, advancing the understanding of epigenetic mechanisms in cancer progression and providing a theoretical foundation for developing METTL3-targeted therapeutic strategies.