MicroRNAs are a class of endogenously expressed small noncoding RNAs that are usually 18,23 nucleotides long, and regulate gene expression posttranscriptionally by targeting the untranslated regions. MiRNAs have been shown to participate in a variety of cellular functions including cell apoptosis, cell proliferation, neural development, and stem cell differentiation. They have been identified as a new kind of gene expression regulators through targeting mRNAs for translational repression or degradation. Gliomas are the most common type of primary brain tumors in adults. Among gliomas, astrocytomas have the highest incidence. According to World Health Organization’s classification, astrocytomas are divided into four grades: pilocytic astrocytoma, diffuse astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme. Anaplastic astrocytoma and glioblastoma multiforme are considered malignant glioma. Recently, many miRNAs are found to play important roles in glioma. MiR-7 was down-regulated in glioblastoma which inhibited invasiveness of primary glioblastoma lines, while miR-26 promotes glioblastoma cell proliferation in vitro and tumor growth in vivo by targeting several tumor suppressor genes such as PTEN and RB1. MiR-128 is a brain-enriched miRNA. Most of the studies of miR-128 in carcinogenesis are focusing on glioma. For example, miR-128 has been shown to be downregulated in glioma. Overexpression of miR-128 inhibits cell proliferation by targeting E2F3a and Bmi-1,Etidronate and reduces neuroblastoma cell motility and invasiveness through inhibiting Reelin and DCX. However, further investigation needs to be performed to elucidate the role of miR-128 in carcinogenesis and tumor development of glioma. P70S6K1 is one of the key downstream targets of mammalian target of rapamycin, which plays important roles in cancerous characteristics such as cell cycle, Pantoprazole sodium cell growth and proliferation. Growing evidence indicates that p70S6K1 pathway is involved in carcinogenesis, metastasis and chemotherapeutic drug resistance. Our previous studies have demonstrated that mTOR/p70S6K1 is involved in regulating tumor angiogenesis and tumorigenesis. Tumor angiogenesis is required for tumor development and growth. Vascular endothelial growth factor is considered to be the most important growth factor among the angiogenic factors. Hypoxia-inducible factor 1 is one of the major regulator of VEGF. High levels of HIF-1 expression are observed in many human cancers, and correlated with tumorigenesis. P70S6K1 is implicated in regulating HIF-1a expression. However, it is unclear what miRNAs directly regulate p70S6K1 in glioma. In the present study, we found that miR-128 was downregulated in human glioma and acted as a tumor suppressor by directly targeting p70S6K1. Forced expression of miR-128 inhibited p70S6K1, HIF-1a, and VEGF expression. Overexpression of p70S6K1 restored miR-128-inhibited HIF-1a and VEGF expression, confirming that p70S6K1 is the downstream target of miR-128. In addition, miR-128 overexpression suppressed cell proliferation and attenuated tumor growth and angiogenesis in vivo. These results give novel insights into our understanding the role and mechanism of miR-128 in glioma pathoetiology, and provide a potential therapeutic strategy for glioma treatment in the future. This study procedure was approved by The Institutional Review Board at the hospital. All participants provided written informed consent. Tissue samples were collected during surgery. For each sample, the major portion of tissue was frozen immediately in liquid nitrogen for molecular analysis, and the remaining tissue was fixed in paraformaldehyde for histological examination.