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MicroRNA-106b (miR-106b) is a highly conserved non-coding RNA that belongs to the miR-106b-25 cluster located on human chromosome 7 [NCBI: Gene ID 406900]. It functions as a critical post-transcriptional regulator by binding to the 3' untranslated regions (UTRs) of various target mRNAs, most notably tumor suppressors such as CDKN1A (p21), PTEN, and RB1 [PubMed: 19233796]. In the context of oncology, miR-106b is frequently overexpressed and acts as an oncomiR, promoting cell cycle progression, epithelial-mesenchymal transition (EMT), and resistance to apoptosis in cancers such as gastric, breast, and hepatocellular carcinoma [PubMed: 25664171, PubMed: 21464214]. Beyond cancer, it has been implicated in neurodegenerative processes, particularly Alzheimer's disease, where it regulates amyloid precursor protein (APP) expression and Aβ production [PubMed: 22451607]. Therapeutic strategies targeting miR-106b primarily involve the use of antisense oligonucleotides (antagomirs) or locked nucleic acids (LNAs) to sequester the miRNA and restore the expression of its tumor-suppressive targets [PubMed: 26823730].
Antisense oligonucleotides bind to miR-106b through complementary base pairing, preventing it from interacting with its target mRNAs and thus reversing its oncogenic effects [PubMed: 26823730].
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