Objective:To explore the expression levels and mechanisms of methyltransferase-like 3(METTL3)in esophageal squamous cell carcinoma.Methods:In vitro construction of METTL3 knockdown model in Eca-109,validated by quantitative real-time PCR(qRT-PCR)and Western Blot to confirm knockdown levels,and assessment of tumor cell proliferation and migra-tion abilities.Exploring METTL3 target genes through differential analysis,enrichment analysis,and survival analysis.Results:Knocking down METTL3 significantly inhibits the proliferation and migration abilities of esophageal cancer cells.Through bioinformatics analysis,we identified 9 potential target genes regulated by METTL3 spermidine/spermine N1-acetyltransferase 1(SAT1),low density lipoprotein receptor(LDLR),integrin subunit beta 1(ITGB1),intercellular adhesion molecule 5(ICAM5),glutamate-rich WD40 repeat containing 1(GRWD1),fibronectintype-Ⅲ domain-containing protein 3A(FNDC3A),DnaJ heat shock protein family(Hsp40)member C2(DNAJC2),coiled-coil domain containing 88C(CCDC88C),Rho GTPase activating pro-tein 12(ARHGAP12).High expression of SAT1 is closely associated with poor prognosis in esophageal squamous cell carcinoma patients.Conclusions:METTL3 exerts a pro-cancer role in esophageal squamous cell carcinoma,potentially impacting the prognosis of esophageal squamous cell carcinoma patients by regulating m6A methylation of target genes such as SAT1.
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