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microRNA-23b-3p is a small, non-coding RNA molecule approximately 22 nucleotides in length that functions as a critical post-transcriptional regulator of gene expression [1, 8]. It belongs to the miR-23b/27b/24-1 cluster and exerts its biological effects by binding to the 3' untranslated regions of target messenger RNAs, leading to their degradation or translational inhibition [2, 3]. This microRNA is involved in a wide array of cellular processes, including cell proliferation, differentiation, apoptosis, and the immune response [2, 12]. In the context of human disease, microRNA-23b-3p exhibits a complex, context-dependent role; it can function as either a tumor suppressor or an oncogene in various cancers, such as gastric, lung, and breast cancer [1, 4, 5]. Furthermore, it has been identified as a potential therapeutic target in neurodegenerative conditions like Alzheimer's disease, where its downregulation is linked to increased tau hyperphosphorylation via the GSK-3β pathway [7, 9, 10]. Experimental therapeutic approaches currently focus on the use of miRNA mimics to restore its function or antagomirs to inhibit its activity, depending on the disease state [1, 7, 10]. Despite its potential, therapeutic development faces challenges such as off-target effects and the need for efficient delivery systems to specific tissues [1, 10].
Post-transcriptional gene silencing via the RNA-induced silencing complex (RISC) by binding to the 3' UTR of target mRNAs [3, 8]
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