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MicroRNA 2683-3p (miR-2683-3p) is a small, non-coding RNA molecule that serves as a critical post-transcriptional regulator of gene expression. It operates by binding to the 3' untranslated regions (UTRs) of specific messenger RNAs, thereby inhibiting their translation or promoting their degradation. miR-2683-3p has been prominently identified as a key regulator in the lncRNA ITSN1-2/miR-2683-3p/PELI3/RIP2 axis, which is significantly involved in the pathogenesis of rheumatoid arthritis (RA) and gastric cancer. In RA, the sequestration of miR-2683-3p by the lncRNA ITSN1-2 leads to the upregulation of PELI3 (Pellino-3), which in turn modulates RIP2 (RIPK2) ubiquitination and activates NF-κB signaling, driving the migration and invasion of fibroblast-like synovicytes. In oncology, miR-2683-3p is associated with the regulation of cell proliferation and tumor progression, often acting within complex feedback loops involving other non-coding RNAs. While no targeted therapies are currently FDA-approved, experimental strategies such as miRNA mimics and antagomirs are under investigation, and traditional Chinese medicine formulas like Juanbi Qianggu have demonstrated the ability to modulate its regulatory pathways in preclinical models.
MicroRNA 2683-3p functions by binding to the 3' untranslated region (UTR) of target mRNAs, such as PELI3, to induce translational repression or mRNA degradation. In disease states, it can be sequestered by long non-coding RNAs (lncRNAs) like ITSN1-2, which act as competitive endogenous RNAs (ceRNAs) to prevent miR-2683-3p from inhibiting its targets.
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