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hsa-miR-373-3p is a mature microRNA that plays a significant role in the post-transcriptional regulation of gene expression by binding to the 3'-untranslated regions (3'-UTR) of target mRNAs [3, 8]. It is part of the miR-371-373 cluster and is involved in a wide array of biological processes, including cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) [8]. In the context of oncology, miR-373-3p exhibits dual roles; it acts as an oncogene in cancers such as colon and bladder cancer by promoting aerobic glycolysis and invasion, while functioning as a tumor suppressor in non-small cell lung cancer (NSCLC) by targeting the GAB2/PI3K/AKT signaling pathway [2, 6]. Beyond its role in cancer, miR-373-3p is implicated in cardiovascular diseases, such as coronary atherosclerosis, where it regulates angiogenesis by targeting vascular endothelial growth factor A (VEGFA) [9]. It is also being investigated as a potential biomarker in biofluids like serum and cerebrospinal fluid for the diagnosis of germ cell tumors and neurodegenerative conditions [11, 13]. Therapeutic approaches targeting miR-373-3p involve the use of synthetic mimics to restore its activity or antagomirs to inhibit its oncogenic effects, although these strategies face challenges related to delivery efficiency and off-target toxicity [1, 16].
MicroRNAs regulate gene expression by binding to the 3'-untranslated region (3'-UTR) of target messenger RNAs (mRNAs), leading to mRNA degradation or translational repression [3, 8]. hsa-miR-373-3p specifically targets genes such as GAB2, MFN2, VEGFA, and DKK1 to modulate downstream signaling pathways like PI3K/AKT/mTOR and Wnt/beta-catenin [2, 6, 9].
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