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Alpha-fetoprotein (AFP) messenger RNA is the transcript of the AFP gene, which encodes a major plasma protein primarily produced by the yolk sac and fetal liver during embryonic development [5, 10]. While AFP expression is normally silenced shortly after birth, the mRNA is frequently re-expressed at high levels in adult tissues during the development of hepatocellular carcinoma (HCC) and certain germ cell tumors [2, 13]. As a therapeutic target, AFP mRNA is addressed using RNA-based technologies such as small interfering RNAs (siRNAs) and antisense oligonucleotides (ASOs) designed to silence the production of the AFP protein, which is known to promote tumor cell survival, proliferation, and immune escape [11, 16]. Preclinical studies have demonstrated that silencing AFP mRNA can induce apoptosis in cancer cells and synergistically enhance the cytotoxic effects of chemotherapeutic agents like doxorubicin [9, 12]. Furthermore, the detection of AFP mRNA in peripheral blood serves as a sensitive molecular biomarker for predicting tumor recurrence and monitoring the hematogenous spread of malignant cells [15].
RNA interference (RNAi) or antisense inhibition leading to the degradation of the target mRNA transcript via the RNA-induced silencing complex (RISC) or RNase H-mediated cleavage, thereby preventing the translation of the Alpha-fetoprotein protein.
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