Cellular myelocytomatosis oncogene messenger RNA 3′ untranslated region (c-MYC mRNA 3′UTR)

The Cellular myelocytomatosis oncogene (c-MYC) messenger RNA 3′ untranslated region (3′UTR) is a critical regulatory segment of the mRNA transcript for the c-MYC proto-oncogene, a master transcription factor that regulates cell growth, proliferation, and metabolism (Dang, 2012). This region contains various cis-acting elements, including AU-rich elements (AREs) and poly-U sequences, which interact with RNA-binding proteins and microRNAs to control the stability and translation efficiency of the c-MYC transcript (Dejure et al., 2017). In many malignancies, the 3′UTR is exploited to maintain the high levels of c-MYC expression necessary for tumor survival, aggressiveness, and metastasis (Dorji et al., 2025). Because the c-MYC protein itself is historically considered "undruggable" due to its lack of a defined small-molecule binding pocket, the 3′UTR has emerged as a promising alternative therapeutic target (Soucek et al., 2008). Novel therapeutic approaches, such as the mRNA drug 3′UTRMYC1-18, utilize "RNA overwriting" technology to destabilize the transcript and trigger its degradation via nonsense-mediated decay (UTR Therapeutics, 2025). By targeting the mRNA blueprint rather than the protein, these therapies aim to selectively silence c-MYC in cancer cells while minimizing toxicity to normal tissues (Dorji et al., 2025).

Other names

c-MYC 3'UTRMYC 3'UTR3' untranslated region of c-MYC mRNAc-MYC mRNA 3-prime untranslated region

The primary mechanism involves mRNA destabilization and degradation, often through the recruitment of the nonsense-mediated decay (NMD) pathway or by disrupting stabilizing interactions with RNA-binding proteins like HuR and ANXA2 (Dorji et al., 2025; Gao et al., 2004).