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Abstract Background The epithelial-to-mesenchymal transition (EMT) has been linked to the regulation of glioma progression. However, the underlying signaling mechanisms that regulate EMT are poorly understood. Methods Quantitative real-time PCR (RT-qPCR) and western blot were performed to detect the expression of MeCP2 in glioma tissues and cell lines. MeCP2 functions were tested with cell immunofluorescence staining and western blot. For in vivo experiments, mouse xenograft model was used to investigate the effects of MeCP2 on glioma. ChIP and Co-IP were used to detect the relationships among MeCP2, miR-200c and Suv39H1. Results In this study, we found that MeCP2 was frequently up-regulated in human glioma tissues and cell lines. MeCP2 knockdown remarkably induced cell epithelial phenotype and inhibited mesenchymal marker ZEB1 and ZEB2 in vitro and in vivo. In addition, MeCP2 in glioma tissues was negatively correlated with miR-200c expression, and miR-200c overexpression partially abrogated mesenchymal phenotype induced by MeCP2. More importantly, we showed that MeCP2 recruited H3K9 to the promoter of miR-200c by interacting with SUV39H1, resulting in EMT of glioma cells. Conclusions This study for the first time reveals MeCP2 as a novel regulator of EMT in glioma and suggest that MeCP2 inhibition may represent a promising therapeutic option for suppressing EMT in glioma.

The exponential growth in Internet traffic requires a high-capacity transmission platform and emphasizes the importance of a multi-granularity transport network due to heterogeneous connection requests. Elastic Optical Network has been considered as a promising solution because of large transport capacity and bandwidth flexibility. Routing and spectrum allocation is one of important problems in EON. However, with spectrum continuity constraint and contiguity constraint, the set-up and tear-down of light paths may cause fragmentation problem which refers to small-sized and uncontiguous spectrums. The fragmentation increases the connection blocking probability and decrease spectrum utilization. In this paper a novel routing and spectrum allocation algorithm is proposed to minimize fragmentation in EON. The proposed algorithm consists of routing problem and the spectrum allocation problem. In the first step, K-shortest paths algorithm is employed and candidate paths are found according to the distance between source and destination. In the second step, fragmentation-aware spectrum allocation algorithm is applied. We define block cost function to determine appropriate spectral block for connection request. The block cost function is based on the state of neighboring frequency slots to minimize the fragmentation after spectrum allocation. The performance of proposed algorithm is evaluated in terms of blocking probability and spectrum utilization.