MicroRNA 1825 (miR-1825) (miR-1825)

MicroRNA 1825 (miR-1825) is a small, non-coding RNA molecule that functions as a post-transcriptional regulator of gene expression by binding to the 3'-untranslated regions (3'-UTRs) of multiple target messenger RNAs (mRNAs). By facilitating the degradation of these mRNAs or inhibiting their translation, miR-1825 modulates various cellular pathways, including those involved in cytoskeletal dynamics and cell cycle progression (Helferich et al., 2018, Scientific Reports). In clinical contexts, miR-1825 has been identified as a significant factor in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS), where its downregulation leads to the overexpression of Tubulin Folding Cofactor B (TBCB), resulting in microtubule instability and motor neuron degeneration (Helferich et al., 2018, Scientific Reports). Beyond neurodegeneration, miR-1825 is implicated in oncology, where it can act as a tumor suppressor or oncogene depending on the malignancy, and in regenerative medicine, where it has been shown to promote cardiomyocyte proliferation following myocardial injury (Hu et al., 2020, Molecular Therapy - Nucleic Acids). While there are currently no FDA-approved drugs specifically targeting miR-1825, experimental approaches using miRNA mimics to restore its function or antagomirs to inhibit it are being explored. The therapeutic development of miR-1825-based interventions faces challenges such as ensuring precise delivery to target tissues and minimizing off-target effects due to the miRNA's ability to regulate multiple genes simultaneously (Zhang et al., 2020, Frontiers in Oncology).

Other names

MIR1825hsa-miR-1825MIRN1825

miR-1825 binds to the 3'-untranslated regions (3'-UTRs) of target mRNAs to induce gene silencing via the RNA-induced silencing complex (RISC), leading to mRNA degradation or translational repression.