MicroRNA-150-5p-mediated Inhibition of Cell Proliferation, G1/S Transition, and Migration in Bladder Cancer through Targeting NEDD4-binding Protein 2-like 1 Gene.

MicroRNA-150-5p (miR-150-5p) has been implicated in the progression of several cancer types, yet its specific functional role and regulatory mechanisms in bladder cancer (BC) remain largely unexplored. Our study revealed significant downregulation of miR-150-5p and upregulation of NEDD4-binding protein 2-like 1 gene (N4BP2L1) in BC tissues compared to controls using quantitative real-time polymerase chain reaction and western blot analysis, respectively. Reduced miR-150-5p expression correlated with advanced tumor stage and lymph node metastasis, while increased N4BP2L1 levels were associated with larger tumor size by the Chi-square test. Functionally, miR-150-5p exerted significant inhibitory effects on BC cell proliferation, migration, inducing G0/G1 phase arrest, and apoptosis. We confirmed N4BP2L1 as a direct target of miR-150-5p in BC cells using luciferase reporter assay. Crucially, N4BP2L1 knockdown mimicked, while overexpression counteracted the inhibitory impacts of miR-150-5p on BC cell proliferation, migration, and invasion. In addition, N4BP2L1 overexpression reversed miR-150-5p-induced alterations in CDK4, Cyclin D1, Bcl-2, PCNA, Ki-67, N-cadherin, Bad, and E-cadherin levels in BC cells. Based on these results, it can be inferred that the miR-150-5p/N4BP2L1 axis might constitute a promising candidate for therapeutic targeting in the treatment of BC.

MiR-592 represses FOXO3 expression and promotes the proliferation of prostate cancer cells.

Prostate cancer (PC) is a serious health problem all over the world. Cell proliferation plays a major role in the tumorigenesis of PC. It is reported that microRNAs (miRNAs) played crucial roles in the regulation of cell proliferation. However, the underlying mechanism of miRNAs in PC has not been intensively investigated. In the present study, the effect of miR-592 on the cell proliferation of PC was investigated. The results showed that miR-592 was significantly upregulated in PC cell and PC tissues. To investigate the biological roles of miR-592, we induced either the up- or downregulation of miR-592 expression by transfecting DU145 PC cells with miR-592 mimics or miR-592 inhibitor. Our results demonstrated that the upregulation of miR-592promoted cell growth, while miR-592 inhibitor showed the opposite effect. Further experiment revealed that miR-592 repressed the expression of FOXO3 by directly targeting the 3'UTR of the FOXO3 transcript, which resulted in upregulating of the expression of cyclin D1 and downregulating of the expression of p21. In sum, our data indicated a novel aspect of the miR-592 in the molecular etiology of PC.