Our findings showed that OM could reverse the remarkable decrease of E-cadherin and SnoN and significantly increase α-SMA, FN, TGF-β1, Arkadia, p-Smad2 and p-Smad3 and remarkly attenuate the ubiquitin-dependent degradation of SnoN induced by high glucose, which indicates that OM can inhibit EMT induced by high glucose via inhibiting TGF-β1/Smad signaling pathway by reducing ubiquitin-dependent degradation of SnoN. The gene discussed is CDH1; the disease is ocular melanoma.