Nivoi FAS-AS1 koreliraju obrnuto sa proizvodnjom sFas, a vezivanje FAS-AS1 za RBM5 inhibira preskakanje egzona 6 posredovano RBM5. EZH2, često mutiran ili prekomjerno eksprimiran u limfomima, hipermetilira promotore FAS-AS1 i potiskuje ekspresiju FAS-AS1. EZH2-posredovana represija FAS-AS1 promotora može se osloboditi DZNeP-om (3-deazaneplanocin A) ili prevladati ektopnom ekspresijom FAS-AS1, što povećava nivo FAS-AS1 i shodno tome smanjuje ekspresiju sFas. Liječenje Brutonovim inhibitorom tirozin-kinaze ili EZH2 snižavanjem, smanjuje razinu EZH2, RBM5 i sFas, čime se pojačava Fas-posredovana apoptoza. Ovo je prvi izvještaj koji prikazuje funkcionalnu regulaciju Fas represije svojom antisens RNK. Dobijeni rezultati otkrivaju nove terapijske ciljeve u limfomima i daju obrazloženje za upotrebu inhibitora EZH2 ili ibrutiniba u kombinaciji s hemoterapijskim agensima koji regrutiraju Fas za učinkovito ubijanje ćelija raka.
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