Bioinformatic analysis of the potential molecular mechanism of PAK7 expression in glioblastoma

The present study aimed to determine the potential molecular mechanisms underlying p21 (RAC1)-activated kinase 7 (PAK7) expression in glioblastoma (GBM) and evaluate candidate prognosis biomarkers for GBM. Gene expression data from patients with GBM, including 144 tumor samples and 5 normal brain samples, were downloaded. Long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) were explored via re-annotation. The differentially expressed genes (DEGs), including differentially expressed mRNAs and differentially expressed lncRNAs, were investigated and subjected to pathway analysis via gene set enrichment analysis. The miRNA-lncRNA-mRNA interaction [competing endogenous RNA (ceRNA)] network was investigated and survival analysis, including of overall survival (OS), was performed on lncRNAs/mRNAs to reveal prognostic markers for GBM. A total of 954 upregulated and 1,234 downregulated DEGs were investigated between GBM samples and control samples. These DEGs, including PAK7, were mainly enriched in pathways such as axon guidance. ceRNA network analysis revealed several outstanding ceRNA relationships, including miR-185-5p-LINC00599-PAK7. Moreover, paraneoplastic antigen Ma family member 5 (PNMA5) and somatostatin receptor 1 (SSTR1) were the two outstanding prognostic genes associated with OS. PAK7 may participate in the tumorigenesis of GBM by regulating axon guidance, and miR-185-5p may play an important role in GBM progression by sponging LINC00599 to prevent interactions with PAK7. PNMA5 and SSTR1 may serve as novel prognostic markers for GBM.