Characterization of genes, down-regulated in human glioma, potential tumor suppressor genes

Dmitrenko, V. V.; Bojko, O. I.; Shostak, K. O.; Vitak, Nazarii; Bukreeva, T. V.; Rozumenko, Volodymyr; Малышева, Т. А.; Shamayev, M. I.; Zozulya, Yuriy; Kavsan, V. M.

doi:10.7124/bc.000773

Cited by 6 publications

(4 citation statements)

References 37 publications

(32 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Evidence demonstrated that CPNE6 terminated their expression in glioblastomas [ 31 ]. Sim and colleagues found that HAPLN2, also known as BRAL1, was virtually absent in malignant gliomas [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA

Yang

Wang

Wei

et al. 2018

BioMed Research International

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA

Yang

Wang

Wei

et al. 2018

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…A previous study established that CCK-8s and CCK-33 directly stimulate human glioma cell growth and invasion process ( 28 ). Also, CCK is downregulated in glioblastoma compared with normal human brain tissues and may function as a TSG in human glioma ( 30 ). By contrast, the present study found that GAST and CCK were significantly associated with GPCR signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of the molecular mechanism of diffuse intrinsic pontine glioma

Deng¹,

Xiong²,

Luo³

et al. 2016

Oncology Letters

View full text Add to dashboard Cite

The present study aimed to elucidate key molecular mechanisms in the progression of diffuse intrinsic pontine glioma (DIPG). The gene expression profile GSE50021, which consisted of 35 pediatric DIPG samples and 10 normal brain samples, was downloaded from the Gene Expression Omnibus database. The differentially-expressed genes (DEGs) in the pediatric DIPG samples were identified. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathways of DEGs were enriched and analyzed. The protein-protein interaction (PPI) network of the DEGs was constructed and functional modules of the PPI network were disclosed using ClusterONE. A total of 679 DEGs (454 up- and 225 downregulated) were identified in the pediatric DIPG samples. DEGs were significantly enriched in various GO terms, and KEGG and Reactome pathways. The PPI network of upregulated (153 nodes and 298 connections) and downregulated (71 nodes and 124 connections) DEGs, and two crucial modules, were obtained. Downregulated genes in module 2, such as cholecystokinin (CCK), gastrin (GAST), adenylate cyclase 2 (brain) (ADCY2) and 5-hydroxytryptamine (serotonin) receptor 7 (HTR7), were significantly enriched in the calcium signaling pathway, the neuroactive ligand-receptor interaction pathway and in GO terms, such as the G-protein coupled receptor (GPCR) signaling pathway, while upregulated genes in module 1 were not enriched in any pathways or GO terms. CCK and GAST associated with the GPCR signaling pathway, HTR7 enriched in the neuroactive ligand-receptor interaction, and ADCY2 and HTR7 involved in the calcium signaling pathway may be key mechanisms playing crucial roles in the development and progression of DIPG.

show abstract

“…Additionally, NAV2 induces neurite outgrowth and is highly expressed in neuroblastoma cells, uterine endometrial stromal sarcoma and colorectal cancer [ 120 ]. MAPK8IP plays an anti-apoptotic role [ 121 ] and showed decreased expression level in glioblastoma [ 122 ]. The protein kinase SYK has been described as tumor suppressor in breast and glial cells [ 123 ].…”

Section: Introductionmentioning

confidence: 99%

The untold stories of the speech gene, the FOXP2 cancer gene

Herrero

Gitton

2018

Genes Cancer

View full text Add to dashboard Cite

FOXP2 encodes a transcription factor involved in speech and language acquisition. Growing evidence now suggests that dysregulated FOXP2 activity may also be instrumental in human oncogenesis, along the lines of other cardinal developmental transcription factors such as DLX5 and DLX6 [1–4].Several FOXP familymembers are directly involved during cancer initiation, maintenance and progression in the adult [5–8]. This may comprise either a pro-oncogenic activity or a deficient tumor-suppressor role, depending upon cell types and associated signaling pathways. While FOXP2 is expressed in numerous cell types, its expression has been found to be down-regulated in breast cancer [9], hepatocellular carcinoma [8] and gastric cancer biopsies [10]. Conversely, overexpressed FOXP2 has been reported in multiple myelomas, MGUS (Monoclonal Gammopathy of Undetermined Significance), several subtypes of lymphomas [5,11], as well as in neuroblastomas [12] and ERG fusion-negative prostate cancers [13]. According to functional evidences reported in breast cancer [9] and survey of recent transcriptomic and proteomic analyses of different tumor biopsies, we postulate that FOXP2 dysregulation may play a main role throughout cancer initiation and progression. In some cancer conditions, FOXP2 levels are now considered as a critical diagnostic marker of neoplastic cells, and in many situations, they even bear strong prognostic value [5]. Whether FOXP2 may further become a therapeutic target is an actively explored lead. Knowledge reviewed here may help improve our understanding of FOXP2 roles during oncogenesis and provide cues for diagnostic, prognostic and therapeutic analyses.

show abstract

Characterization of genes, down-regulated in human glioma, potential tumor suppressor genes

Cited by 6 publications

References 37 publications

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA

Bioinformatics analysis of the molecular mechanism of diffuse intrinsic pontine glioma

The untold stories of the speech gene, the FOXP2 cancer gene

Contact Info

Product

Resources

About