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Long non-coding RNAs (lncRNAs) have recently emerged as a major class ofregulatory molecules involved in a broad range of biological processes and complexdiseases. Our aim was to identify important lncRNAs that might play an importantrole in contributing to glioblastoma (GBM) pathogenesis by conducting lncRNA andmRNA prole comparison between GBM and normal brain tissue. The differentiallyexpressed lncRNA and mRNA proles of the tissue between GBM patient and age-matcheddonor without GBM diseases were analyzed using microarrays. We propose a novelmodel for the identification of lncRNA-mRNA targeting relationships that combinethe potential targets of the differentially expressed lncRNAs with the differentiallyexpressed mRNA abundance data. Bioinformatic analysis of the predicted targetgenes (gene ontology, pathway and network analysis) was performed for furtherresearch. The lncRNA microarray reveals differentially expressed lncRNAs betweenGBM and normal brain tissues. In the GBM group, 654 lncRNAs were upregulated and654 were downregulated (fold change ≥4.0 or ≤0.25, P&lt;0.01). We found 104 matchedlncRNA-mRNA pairs for 91 differentially expressed lncRNAs and 84 differentiallyexpressed genes. Target gene-related pathway analysis showed signicant changesin PPAR pathways in the GBM group compared with the normal brain group (P&lt;0.05).By further conducting lncRNA gene network analysis, we found that ASLNC22381 andASLNC2081 were likely to play roles in the regulation of glioma signaling pathways.In conclusion, our results indicated that the lncRNA expression prole in GBMtissue was signicantly altered. These results may provide important insightsinto the mechanisms responsible for GBM progression and pathogenesis. This studyalso suggests that ASLNC22381 and ASLNC20819 may play important roles via theirtarget IGF-1 in the recurrence and malignant progression of GBM.

LncRNA proﬁle of glioblastoma reveals the potential role of lncRNAs in contributing to glioblastoma pathogenesis