(Figures 7C and 7D), indicating that miR-128 attenuated glioma cell-inducing angiogenesis. Furthermore, we selected four cases in every grade of glioma tissues, and analyzed the number of CD31- positive microvessels in glioma specimens, the normal brain tissues were used as negative control. As shown in Figure 7E, the number of CD31-positive microvessels was much lower in normal brain tissue sections than those in glioma specimens. We analyzed CD31-positive microvessel density and miR-128 expression levels in the glioma tissues using SPSS software, and found that there is a significant inverse correlation of miR-128 levels and the CD31- positive microvessel densities in glioma tissues with Spearman’s correlation, r = 20.673 (P,0.05). Discussion MiRNAs function as post-transcriptional gene regulators in regulating various physiological and pathological events [33]. MiRNA abnormalities are thought to play important roles in cancer development. Recent studies have showed that many miRNAs are down-regulated in tumors when compared to normal tissues [34]. Consistent with previous studies [9,10], we demon- strated that the expression of miR-128 in glioma tissues was down- regulated when compared to normal brain tissues. The results indicate that miR-128 is involved in pathogenesis of glioma. To determine the role and molecular mechanism of miR-128 in glioma development, we used computational bioinformatics to predict the potential targets of miR-128. Among the potential targets, we confirmed that p70S6K1 is a novel target of miR-128 by experimental method with forced expression of miR-128 suppressing p70S6K1 protein expression. In agreement with these results, overexpression of p70S6K1 rescued the inhibitory effect of miR-128 on p70S6K1 signaling pathway. Interestingly, the levels of miR-128 were negatively correlated with p70S6K1 protein levels in glioma tissues. Thus, this study is useful not only to reveal References 1. 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