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MicroRNA 193b-3p (miR-193b-3p) is a small, non-coding RNA molecule that plays a critical role in the post-transcriptional regulation of gene expression. It is derived from the MIR193B gene and functions by binding to the 3' untranslated regions (UTRs) of target messenger RNAs, leading to their degradation or the inhibition of their translation [1, 6]. In the context of oncology, miR-193b-3p is predominantly characterized as a tumor suppressor, frequently downregulated in various malignancies such as lung, breast, and esophageal cancers [1, 3, 4]. By targeting key oncogenic drivers like Cyclin D1 (CCND1) and MYB, it effectively inhibits cell proliferation, migration, and invasion while promoting apoptosis [1, 5, 8]. However, its biological role is context-dependent, as it has been observed to act as an oncomiR in certain conditions, such as glioma [11]. Beyond cancer, miR-193b-3p is involved in metabolic regulation, neuroprotection, and the response to cardiovascular injury, making it a versatile biomarker and therapeutic target [3, 13, 15]. Therapeutic approaches currently focus on the delivery of miRNA mimics to restore its suppressive function or antagomirs to block its activity in specific disease states [3, 4].
miR-193b-3p functions through RNA interference by binding to the 3' untranslated region (3'UTR) of target mRNAs, such as CCND1, MYB, and RSF1, resulting in mRNA degradation or translational repression [1, 4, 5].
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