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Oncogenic messenger RNA (mRNA) refers to the transcript of a gene that has the potential to cause cancer when overexpressed or mutated [1, 7]. These mRNAs serve as the essential intermediate templates for the translation of oncogenic proteins, such as KRAS, MYC, or STAT3, which drive uncontrolled cell proliferation, survival, and metastasis [6, 13]. In modern pharmacology, oncogenic mRNA is a primary target for 'informational' drugs, including antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) [2, 3]. These therapeutic agents are designed with a sequence complementary to the target mRNA, allowing them to bind with high specificity [1, 6]. This binding typically leads to the degradation of the mRNA via enzymes like RNase H or the RNA-induced silencing complex (RISC), or prevents its translation by the ribosome, thereby silencing the expression of the disease-causing protein [3, 7]. The term 'Complementary oncogenic mRNA' is considered incorrect as a canonical name because it describes the relationship between the drug and the target rather than the target itself [1, 2].
Antisense oligonucleotides (ASOs) or small interfering RNA (siRNA) molecules bind to the target oncogenic mRNA via Watson-Crick base pairing, leading to mRNA degradation (mediated by RNase H or the RISC complex) or translational blockade, thereby preventing the synthesis of the encoded oncoprotein.
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