Myc proto-oncogene mRNA (MYC mRNA)

Myc proto-oncogene mRNA is the primary transcript of the MYC gene, which encodes the c-Myc protein, a master transcription factor essential for coordinating cell growth, metabolism, and cell cycle progression [12, 15]. It acts as a global regulator of gene expression, influencing approximately 15% of the human genome and facilitating the rapid proliferation required for normal development and tissue repair [12, 14]. In the context of cancer, this mRNA is frequently overexpressed or stabilized through mechanisms such as gene amplification, chromosomal translocations, or dysregulated signaling pathways [6, 17]. This deregulation drives the hallmark metabolic reprogramming and unchecked division seen in a wide array of malignancies, including Burkitt lymphoma, breast, and lung cancers [3, 9, 15]. Because the c-Myc protein lacks a traditional enzymatic active site or binding pocket, it has historically been considered undruggable, leading researchers to target its mRNA as an alternative therapeutic strategy [5, 16]. Various modalities, including antisense oligonucleotides (ASOs), small interfering RNAs (siRNAs), and small molecules targeting mRNA G-quadruplexes or translation factors, are designed to induce transcript degradation or block protein synthesis [5, 7, 18]. While candidates like IONIS-MYC-2.5Rx and DCR-MYC have entered clinical trials, significant hurdles remain, including the efficient delivery of RNA-targeting agents and the potential for on-target toxicity in proliferative normal tissues like the bone marrow [1, 16]. Monitoring MYC mRNA levels and gene status serves as a critical biomarker for identifying patients likely to benefit from these targeted interventions [1, 3, 6].

Other names

c-myc mRNAc-Myc oncogene mRNAv-myc avian myelocytomatosis viral oncogene homolog mRNAMYC messenger RNA

Therapeutic inhibition is achieved through antisense oligonucleotide-mediated RNase H cleavage of the mRNA, RNA interference-mediated transcript degradation, or steric blocking of translation via small molecules, morpholinos, or the stabilization of inhibitory G-quadruplex structures [5, 7, 16, 18].