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  • Title: Tumor suppressor miR-361-3p inhibits prostate cancer progression through Gli1 and AKT/mTOR signaling pathway.
    Author: Wang S, Huang X, Zhang G, Chen Z, Guan H, Zhou W.
    Journal: Cell Signal; 2024 Feb; 114():110998. PubMed ID: 38048859.
    Abstract:
    BACKGROUND: The primary challenge in prostate cancer (PCa) is tumor metastasis, which seriously affects the survival time of patients. Growing evidence suggests that microRNAs play a crucial regulatory role in various malignancies and that the tumor suppressor miR-361-3p is responsible for regulating migration, proliferation, and invasion in different cancer types. However, the underlying regulatory mechanism of miR-361-3p in PCa remains unknown. METHODS: The expression of miR-361-3p in PCa cells was analyzed using quantitative real time-polymerase chain reaction. The clinical utility of miR-361-3p in PCa was evaluated using in vitro assays. The mechanism of action of miR-361-3p was investigated using western blotting, luciferase reporter assays, immunofluorescence, and rescue studies. RESULTS: The function, invasiveness, migration, and proliferation of PCa cells, as well as epithelial-mesenchymal transition (EMT), were aided by the downregulation of miR-361-3p, whereas its overexpression exerted the opposite effect. Repression of glioma-associated oncogene homolog 1 (Gli1) expression by miR-361-3p led to activation of the protein kinase B/mammalian target of rapamycin (AKT/mTOR) signaling pathway, triggering EMT and promoting PCa metastasis. CONCLUSIONS: Downregulation of miR-361-3p along the Gli1 axis promoted tumor malignancy. Collectively, the results of this study imply that miR-361-3p has the potential to be both a biomarker and therapeutic target in PCa.
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