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The C-Myc-binding protein (MYCBP) mRNA 3'-untranslated region (3'-UTR) is a critical regulatory segment of the transcript encoding the MYCBP protein, also known as AMY-1 [1]. MYCBP acts as a co-activator for the MYC proto-oncogene, binding to its N-terminal transactivation domain to enhance the expression of genes that drive cell cycle progression and oncogenesis [2]. The 3'-UTR of MYCBP contains specific binding sites for several microRNAs, including miR-26a, miR-22, and miR-136, which function as tumor suppressors by inhibiting MYCBP translation or promoting mRNA decay [3][4]. In various malignancies, such as gastric and hepatocellular carcinoma, these microRNAs are frequently downregulated, leading to the overexpression of MYCBP and subsequent hyperactivation of the MYC signaling pathway [5]. Consequently, the MYCBP mRNA 3'-UTR is an emerging therapeutic target for RNA-based strategies, such as miRNA mimics or antisense oligonucleotides, aimed at restoring post-transcriptional repression [6]. By reducing MYCBP levels, these interventions indirectly suppress MYC activity, offering a potential solution for targeting the notoriously "undruggable" MYC pathway [7]. However, the clinical development of such therapies faces challenges including the need for precise delivery systems and the mitigation of off-target effects on other transcripts [6].
RNA interference or antisense-mediated degradation and translational inhibition of the MYCBP transcript [3][6].
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