[No authors listed]
OBJECTIVE:The purpose of this study was to explore the mechanism of microRNA-224 (miR-224) in NSCLC. PATIENTS AND METHODS:Quantitative RT-PCR (qRT-PCR) was used to evaluate expression levels of miR-224. The association of miR-224 with the clinicopathologic features of NSCLC was evaluated in 56 patients. The roles of miR-224 in cell proliferation were analyzed in vivo and in vitro with pre-miR-224 transfected cells. Also, the regulation of RASSF8 by miR-224 was evaluated by qRT-PCR, Western blotting and luciferase reporter assays. RESULTS:In this study, we identified miR-224 to be significantly up-regulated in NSCLC tissues and associated with tumor size. Increased miR-224 expression promotes NSCLC cell proliferation by down-regulating RASSF8 at the mRNA and protein levels. The AKT pathway was found aberrantly activated after over-expression of miR-224. RASSF8 was identified as a direct target of miR-224 by bioinformatics analysis and luciferase reporter assay. CONCLUSIONS:The miR-224 played an oncogenic role in the proliferation of NSCLC by direct targeting RASSF8, and it is suggested that miR-224 may be a potential therapeutic target for NSCLC.
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