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Mature human microRNA miR-363-3p (hsa-miR-363-3p) is a small non-coding RNA molecule that plays a critical role in post-transcriptional gene regulation. It is part of the miR-106a-363 cluster, a paralog of the well-known oncogenic miR-17-92 cluster. miR-363-3p functions by binding to the 3' untranslated regions (UTRs) of specific messenger RNAs, leading to their degradation or translational inhibition. Its biological impact is highly context-dependent; it acts as a tumor suppressor in cancers such as colorectal, lung, and liver cancer by targeting genes like SOX4, PCNA, and HMGA2. Conversely, it can function as an oncomiR in T-cell acute lymphoblastic leukemia and breast cancer by suppressing tumor suppressors like PTEN. Beyond oncology, miR-363-3p is a significant regulator in cardiovascular and renal health, where it modulates endothelial injury and fibrosis by targeting NOX4 and KLF2. In cardiovascular contexts, its upregulation is associated with acute myocardial infarction, making it a potential diagnostic biomarker. Due to its dysregulation in various pathologies, it is being explored as a therapeutic target using miRNA mimics to restore function or antagomirs to inhibit its activity. Therapeutic development faces challenges such as off-target effects and the need for efficient delivery systems to specific tissues.
Post-transcriptional gene silencing by binding to the 3' untranslated region (UTR) of target mRNAs, leading to translational repression or mRNA cleavage.
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