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pmid:30356407

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA.

Qi Yang · Rui Wang · Bo Wei · Chuangang Peng · Le Wang · Guozhang Hu · Daliang Kong · Chao Du

BioMed research international · 2018 doi:10.1155/2018/4246703

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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title
Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA.
doi
10.1155/2018/4246703
pmid
30356407
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[0]
Qi Yang
[1]
Rui Wang
[2]
Bo Wei
[3]
Chuangang Peng
[4]
Le Wang
[5]
Guozhang Hu
[6]
Daliang Kong
[7]
Chao Du
journal
BioMed research international
year
2018
abstract
To reveal the potential molecular mechanism of glioblastoma multiforme (GBM) and provide the candidate biomarkers for GBM gene therapy. Microarray dataset GSE50161 was obtained from GEO database. The differentially expressed genes (DEGs) were identified between GBM samples and control samples, followed by the module partition analysis based on WGCNA. Then, the pathway and functional enrichment analyses of DEGs were performed. The hub genes were further investigated, followed by the survival analysis and data validation. A total of 1913 DEGs were investigated between two groups, followed by analysis of 5 modules using WGCNA. These DEGs were mainly enriched in functions like inflammatory response. The hub genes including upregulated N-Myc and STAT Interactor (NMI), Capping Actin Protein-Gelsolin Like (CAPG), and Proteasome Subunit Beta 8 (PSMB8) were revealed as potential liquid biopsy molecules for GBM diagnose. Moreover, Nucleolar and Spindle Associated Protein 1 (NUSAP1) and G Protein-Coupled Receptor 65 (GPR65) were outstanding genes in survival analysis. Our results suggested that CPNE6, HAPLN2, CMTM3, NMI, CAPG, and PSMB8 might be used as potential molecules for liquid biopsy of GBM. NUSAP1 and GPR65 might be novel prognostic targets for GBM gene therapy. Furthermore, the upregulated NMI might play an important role in GBM progression via inflammatory response.
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Then, the survival rate estimation and statistical significance were performed using Kaplan-Meier (KM) method [23] and log-rank test [24], respectively.
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Then, the survival rate estimation and statistical significance were performed using Kaplan-Meier (KM) method [23] and log-rank test [24], respectively.
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RNA expression patterns in serum microvesicles from patients with glioblastoma multiforme and controls
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The differentially expressed genes (DEGs) were identified between GBM samples and control samples, followed by the module partition analysis based on WGCNA. Then, the pathway and functional enrichment analyses of DEGs were performed. The hub genes were further investigated, followed by the survival analysis and data validation. A total of 1913 DEGs were investigated between two groups, followed by analysis of 5 modules using WGCNA. These DEGs were mainly enriched in functions like inflammatory response. The hub genes including upregulated N-Myc and STAT Interactor (NMI), Capping Actin Protein-Gelsolin Like (CAPG), and Proteasome Subunit Beta 8 (PSMB8) were revealed as potential liquid biopsy molecules for GBM diagnose. Moreover, Nucleolar and Spindle Associated Protein 1 (NUSAP1) and G Protein-Coupled Receptor 65 (GPR65) were outstanding genes in survival analysis. 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