Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0017636 (
glioblastoma
)
18,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
This study was aimed to identify hub genes associated with the development of
glioblastoma
(
GBM
) by conducting a bioinformatic analysis. The raw gene expression data were downloaded from the Gene Expression Omnibus database and The Cancer Genome Atlas project. After the differentially expressed genes (DEGs) were identified, the functional enrichment analysis of DEGs was conducted. Subsequently, the protein-protein interaction (PPI) network, molecular complex detection clusters, and transcriptional factor (TF)-miRNA-target regulatory network were constructed, respectively. Furthermore, the survival analysis of prognostic outcomes and genes was analyzed. In addition, the expression of key genes was validated by quantitative real-time PCR (qRT-PCR) analysis. A total of 884 DEGs, including 418 upregulated and downregulated genes, were identified between
GBM
and normal samples. The PPI network comprised a set of 3418 pairs involving 751 nodes, and
AKT1
and
CDK2
were the critical genes in the network. A total of seven clusters were identified, the genes in which were intensively associated with cell cycle, cholinergic synapse, and extracellular matrix (ECM)-receptor interaction. qRT-PCR analysis indicated that
AKT1
and
CDK2
were significantly upregulated, and
NRXN3
and
NPTX2
were significantly downregulated in
GBM
samples. The TF-miRNA-target regulatory networks were built, in which
CCNB1
,
RFC5
, microRNA524, and microRNA34b were key regulators. There were 43 genes, including
NPTX2
and
NRXN3
, significantly related to the prognostic outcomes of
GBM
patients. These crucial genes might be promising options for
GBM
treatment.
...
PMID:Gene and microRNA Signatures Are Associated with the Development and Survival of Glioblastoma Patients. 3118 28