科研之友
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摘要
Accumulating evidence has demonstrated that B7-H3 is deregulated in several cancers and is closely associated with malignant cell behavior. In the present study, we aimed to explore the expression pattern of B7-H3 and its functional relevance in glioma cells. Real-time PCR and western blotting were performed to detect the mRNA and protein expressions of B7-H3, respectively. Glioma cell growth was measured by CCK-8 and colony formation assays. A luciferase activity assay was used to validate the regulatory mechanism of B7-H3 by microRNA miR-539. CD276 (the gene encoding B7-H3) mRNA and protein levels were elevated significantly in glioma cell lines, including U87 and U251. Downregulation of CD276 mediated by a specific short interfering RNA led to decreased cell proliferation and colony formation in glioma cells. In addition, bioinformatic analysis revealed that CD276 was a potential target of miR-539; this was further validated by a luciferase activity assay. Furthermore, ectopic expression of miR-539 repressed the expression of CD276 and thus inhibited the growth of glioma cells. Taken together, the results showed that miR-539-mediated B7-H3 repression was implicated in glioma cell proliferation, suggesting that regulation of the miR-539/B7-H3 axis might represent a novel therapeutic strategy to treat glioma.
