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microRNA-326 (miR-326) is a highly conserved, small non-coding RNA that serves as a critical post-transcriptional regulator of gene expression [1, 3]. It is located within the first intron of the beta-arrestin 1 (ARRB1) gene on human chromosome 11 [2, 6]. miR-326 primarily functions as a tumor suppressor in various malignancies, such as glioma, non-small cell lung cancer, and breast cancer, by targeting genes involved in cell proliferation, migration, and multidrug resistance, including ABCC1 and SIRT1 [3, 9, 16]. In contrast, it acts as a pro-inflammatory mediator in autoimmune diseases like multiple sclerosis and type 1 diabetes, where its overexpression promotes the differentiation of pathogenic Th17 cells [1, 4]. Therapeutic strategies under investigation include the use of miR-326 mimics to restore its suppressive activity in cancer and antagomirs to inhibit its activity in autoimmune and fibrotic conditions [17, 18, 22]. Additionally, miR-326 has been identified as a potential biomarker for disease diagnosis and prognosis due to its stable presence in peripheral blood and exosomes [1, 8].
miR-326 acts as a post-transcriptional regulator by binding to the 3' untranslated region (UTR) of target mRNAs, leading to translational repression or mRNA degradation. It modulates key signaling pathways such as Notch, Hedgehog, and PI3K/AKT by targeting genes like ABCC1, SIRT1, and ELK1.
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