Abstract
Glioblastoma multiforme (GBM) is the most malignant neuroepithelial primary brain tumor and its mean survival time is 15 months after diagnosis. This study undertook to investigate the genome-wide and transcriptome-wide analyses of human high mobility group box (HMG-box) TF (transcript factor) families / HOX, TOX, FOX, HMG and SOX gene families, and their relationships to GBM. According to the TCGA-GBM profile analysis, differentially expressed HOX, FOX, HMG and SOX gene families (62 DEmRNA) were found in this study. We also analyzed DEmRNA (HMG-box related genes) co-expressed eight DElncRNA in GBM, and constructed a ceRNA network analysis as well. We constructed 50 DElncRNA-DEmiRNA-DEmRNA (HMG-box related genes) pairs between GBM and normal tissues. Then, risk genes SOX6 and SOX21 expression were correlated with immune infiltration levels in GBM. SOX6 also had a strong association with MAPT, GSK3B, FYN and DPYSL4, suggesting that they might be functional members in GBM.
Highlights
Glioblastoma multiforme (GBM) is the most malignant neuroepithelial primary brain tumor [1]
By obtaining data from The Cancer Genome Atlas (TCGA) database, we re-analyze the transcriptomic profiles of TCGA-GBM dataset, and 174 samples (169 GBM tissues and 5 normal tissues) were chosen to obtain differentially expressed mRNAs (DEmRNAs) and DElncRNA
SOX6 compared with MAPT, GSK3B, FYN and DPYSL4 had the highest correlation coefficients (Spearman’s = 0.648, 0.765, 0.693 and 0.642) in GBM compared with other tumors (Figure 9B). This data demonstrated that SOX6 had a strong association with MAPT, GSK3B, FYN and DPYSL4, suggesting that they may be functional partners in GBM
Summary
Glioblastoma multiforme (GBM) is the most malignant neuroepithelial primary brain tumor [1]. HOX gene family was highly expressed in GBM cancer stem cells compared with parental lines, and HOX-PBX inhibition was a potential therapeutic target for GBM patients [5], and HOXD10 was targeted by hsa-miRNA-23a to inhibit glioma cell invasion [6]. SOX6 was expressed by IgGs in GBM [10]. The moderate expression of SOX10 and SOX11 was linked to glioma, whereas the overexpression of them were associated with GBM [11]. SOX9 expression is connected to a poor prognosis of GBM patients and with resistance to temozolomide [12]. FOXG1 and SOX2 via transcriptional control of core cell cycle and epigenetic regulators to fuel unconstrained self-renewal in GBM stem cells [14]. Hsa-miR-338-5p played a tumor suppressor role in glioma by binding FOXD1 [16]
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