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DNA methyltransferase 3 beta (DNMT3B) mRNA is the transcript encoding the DNMT3B enzyme, a key de novo methyltransferase responsible for establishing DNA methylation patterns during early development and cellular differentiation [2, 12]. In various malignancies, such as multiple myeloma and acute myeloid leukemia, DNMT3B is frequently overexpressed, leading to the aberrant hypermethylation and silencing of tumor suppressor genes [1, 6, 9]. Consequently, DNMT3B mRNA is a target for therapeutic intervention, with experimental strategies utilizing small interfering RNAs (siRNAs) or antisense oligonucleotides to reduce its levels and restore gene expression [7, 13, 16]. Beyond oncology, DNMT3B mRNA is being investigated as a therapeutic agent itself; for instance, preclinical studies in osteoarthritis involve the delivery of DNMT3B mRNA to induce protein expression and mitigate joint inflammation [3, 11]. While traditional hypomethylating agents like decitabine and azacitidine target the DNMT3B protein, mRNA-directed therapies offer a more specific approach to modulating epigenetic regulation in disease [7, 11]. Mutations in the DNMT3B gene are also linked to the rare ICF syndrome, highlighting the transcript's importance in maintaining genomic stability [10, 15]. The mRNA also exists in several splice variants, such as DNMT3B3, which may have distinct regulatory roles in different tissues [8, 12].
DNA methyltransferase inhibition, RNA interference-mediated degradation, antisense-mediated knockdown, mRNA-based protein replacement
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