TL;DR
Public database analysis exhibited that lipid metabolism-related gene LGALS3 was upregulated in CRC stem cells and M2 macrophages, providing a highly potential target for CRC.
Clinically, these findings not only deepen the understanding of m6A-mediated posttranscriptional regulation in CRC but also identify this axis as a promising therapeutic target for overcoming ferroptosis resistance and improving patient outcomes.
This study reveals for the first time the complete molecular mechanism by which ZCCHC4-mediated UHRF1 m6A methylation promotes OS progression through epigenetic suppression of CDO1 transcription and inhibition of ferroptosis.
Overexpression of MFN2 suppressed CRC cell glycolysis and tumor growth by enhancing TRIM21-mediated degradation of PFKP andilitation of TRIM21 to PFKP to mediate its degradation, thereby hindering the malignant progression of CRC.
M2-TAMs promote the invasive phenotype of NSCLC cells via upregulating the expression of FGD5-AS1 in NSCLC cells through interaction with miR-22-3p and modulating the expression level of miR-22-3p.
It is demonstrated that lactate derived from CAFs promotes the expression of stemness genes by mediating H3K18 lactylation in the promoters of these genes in NSCLC cells, thereby accelerating the malignant phenotype formation of NSCLC cells.
Clinically, these findings identify the METTL1/USP48/LCN2 pathway as a potential therapeutic target for cSCC and elucidated a novel oncogenic axis in cSCC, wherein METTL1 stabilized USP48 mRNA through m7G methylation modification, and USP48 in turn deubiquitinated and stabilized LCN2 protein.
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