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ObjectiveIn our research we try to explore whether glioma stem cell containing circRNAs signal pathway could regulate glioma malignant progression and elaborate its possible mechanism.MethodsIn this study, we used biological information analysis to build an RNA regulatory network and then proceeded RT-PCR to screen target RNAs, after that we clarified the targeting relationship between circRNA-miRNA-mRNA through double luciferase gene assay, RNA pull down experiment, PCR and Western Blot. Finally we adopted RNA transfection to identify its impact on glioma cell proliferation, invasion, migration, apoptosis and cell cycle.Resultscirc-ASB3 was significantly up-regulated in glioma stem cells compared with glioma cells. The circ-ASB3/miR-543/Twist1 axis was discovered to be a possible regulatory pathway in glioma, circ-ASB3 could adsorb and targeted bind to miR-543, down-regulate miR-543 expression, thus release its targeted inhibition to Twist1. Circ-ASB3 was shown to increase glioma cell proliferation, invasion, and migration in vitro via miR-543/Twist1 axis. Meanwhile glioma cell apoptosis could be inhibited, and cell cycle arrest could be induced through this signaling pathway.Conclusioncirc-ASB3 could enhance glioma malignancy via miR-543/Twist1 axis, resulting in the discovery of new biomarkers and possible therapeutic targets for these patients.

Abstract: The coefficient of thermal expansion (CTE) and accumulated plastic strain of the pure aluminum matrix composite containing 50% SiC particles (Al/SiCp) during thermal cycling (within temperature range 298–573K) were investigated. The composite was produced by infiltrating liquid aluminum into a preform made by SiC particles with an average diameter of 14μm. Experiment results showed that the relationship between the CTE of Al/SiCp and temperature is nonlinear; CTE could reach a maximum value at about 530K. The theoretical accumulated plastic strain of Al/SiCp composites during thermal cycling has also been calculated and compared with the experimental results. [Copyright &y& Elsevier]