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MicroRNA 191 (miR-191) is a highly conserved, small non-coding RNA located within the miR-191/425 cluster on human chromosome 3 (3p21.31). It plays a pivotal role in regulating gene expression post-transcriptionally by binding to the 3' untranslated regions (UTRs) of target mRNAs, leading to translational inhibition or mRNA degradation (Nagpal & Kulshreshtha, 2014). miR-191 is involved in essential biological processes including cell proliferation, apoptosis, and differentiation, particularly within the hematopoietic and epithelial lineages. In oncology, miR-191 is frequently characterized as an "oncomiR" because its overexpression is linked to the progression of various malignancies, such as breast, gastric, and hepatocellular carcinomas, where it promotes the epithelial-mesenchymal transition (EMT) and metastasis (Di Leva et al., 2013). Beyond cancer, miR-191 has been implicated in the pathogenesis of Alzheimer's disease and type 2 diabetes, serving as a potential diagnostic biomarker in liquid biopsies (Kumar et al., 2013). Therapeutic strategies targeting miR-191 primarily involve the use of antisense oligonucleotides (antagomirs) to silence its activity and restore the expression of suppressed tumor suppressor genes like SATB1 and CDK6 (Elyakim et al., 2010). These antisense agents work by sequestering the mature miRNA, preventing its incorporation into the RNA-induced silencing complex (RISC). Despite its potential, therapeutic application faces challenges such as ensuring efficient systemic delivery and minimizing off-target effects on other gene networks.
Antisense inhibition of microRNA activity to restore expression of tumor suppressor target genes.
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