ABSTRACT
OBJECTIVE: To investigate the miR-130b expression in patients with glioma and to analyze its role and underlying molecular mechanism on the carcinogenesis. PATIENTS AND METHODS: The expression levels of miR-130b were detected with quantitative Real-time PCR. The relationship between miR-130b expression and clinicopathologic characteristics were analyzed. MiR-130b inhibitor was transfected into glioma cell lines to investigate its role in HCC. MTT assays were conducted to explore the impact of miR-130b down-expression on the proliferation of human glioma cells. Cell cycle and cell apoptosis assays were performed using flow cytometry. Levels of ERK/MAPK pathway related proteins were evaluated by Western blotting. Data were analyzed using the 2-ΔΔCT method through student's t-test via the GraphPad Prism software (La Jolla, CA, USA). RESULTS: The expression of miR-130b was markedly upregulated in glioma cell lines and tissues, and high miR-130b expression was significantly associated with advanced WHO grade (p = 0.022) and low Karnofsky performance score (p = 0.001). In addition, downregulation of miR-130b inhibited the proliferation of glioma cells and induced cell-cycle arrest and cells apoptosis in vivo. Importantly, ERK/MAPK pathway was found to be inactivated in the glioma cell lines after miR-130b knockout experiment. CONCLUSIONS: The current data indicated that miR-130b may play a critical role in the progression of glioma via ERK/MAPK signaling cascades, suggesting that it may be a useful therapeutic agent in glioma patients.
Subject(s)
Brain Neoplasms/genetics , Glioma/genetics , MAP Kinase Signaling System/genetics , MicroRNAs/genetics , Apoptosis/genetics , Brain Neoplasms/pathology , Cell Cycle/genetics , Cell Line, Tumor , Cell Proliferation/genetics , Gene Expression Regulation, Neoplastic , Glioma/pathology , Humans , Male , Real-Time Polymerase Chain Reaction , Up-RegulationABSTRACT
OBJECTIVE: MicroRNAs (miRNAs) have been widely studied as a potential cancer agent, but its efficacy does not get improvement due to poor targeting. miRNAs have been reported to play multiple roles in the development of the tumor. miR-124 is expressed in various tumor. This study aimed to elucidate the expression of miR-124 in neuroglioma cells as well as its related mechanism. MATERIALS AND METHODS: Expression of miR-124 in neuroglioma cells was assessed by Quantitative PCR (q-PCR). Astrocytes (RA cells) were used as control group. The relationship between miR-124 and SCP-1 was explored with bioinformatics tools. Luciferase reporter assay was performed to examine the expression of miR-124 target protein SCP-1. Gene interference technology was used to regulate expression of miR-124 and SCP-1 in neuroglioma cells, and q-PCR was performed to confirm gene interference effects. Migration of miR-124 and SCP-1 in neuroglioma cell was measured by wound healing assay and cell migration test. RESULTS: Compared with control group, the expressions of miR-124 (p=0.0015) and SCP-1 (p=0.0042) were higher in neuroglioma cells. Luciferase reporter assay proved that SCP-1 was the target of miR-124. Wound healing assay and migration test showed down-regulation of SCP-1 inhibited neuroglioma cell migration. Down-regulation of miR-124 didn't influence neuroglioma cell migration movement. CONCLUSIONS: miR-124 and SCP-1 in neuroglioma cell were highly expressed. MiR-124 impeded the progression of neuroglioma via down-regulating SCP-1.
