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pmid:34797290

DDX10 and BYSL as the potential targets of chondrosarcoma and glioma.

Xuemin Quan · Changsong Zhao · Zhengrong Gao · Yao Zhang · Rugang Zhao · Jingjing Wang · Qiang Zhang

Medicine · 2021 doi:10.1097/MD.0000000000027669

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

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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pmid:34797290
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title
DDX10 and BYSL as the potential targets of chondrosarcoma and glioma.
doi
10.1097/MD.0000000000027669
pmid
34797290
authors array · 7 items
[0]
Xuemin Quan
[1]
Changsong Zhao
[2]
Zhengrong Gao
[3]
Yao Zhang
[4]
Rugang Zhao
[5]
Jingjing Wang
[6]
Qiang Zhang
journal
Medicine
year
2021
abstract
ABSTRACT: To provide reliable molecular markers and effective therapeutic targets for chondrosarcoma and glioma.Gene Set Enrichment (GSE) 29745 and GSE48420 were downloaded from the Gene Expression Omnibus (GEO) database. Differently expressed genes (DEGs) were identified by the GEO2R. We annotated the function of common DEGs through Digital Audio/Video Interactive Decoder (DAVID) and Metascape. Protein-protein interaction network construction was performed through STRING. Hub genes were identified by the two different algorithms (MCC, EPC). DDX10 and BYSL were key factors in embryo implantation and development, and plays a role in a variety of cancers. The role of the DDX10 and BYSL on the glioma derived from the chondrosarcoma would be explored by the clinical samples.A total of 1442 DEGs were identified. The variations in DEGs were mainly enriched in vasculature development, cell motion, blood vessel development, cell migration, regulation of cell proliferation, regulation of cell proliferation, wound healing, biological adhesion, growth factor binding, identical pathways in cancer, and p53 signaling pathway. Dead-box helicase 10 (DDX10), Bystin-like (BYSL), and WD repeat domain 12 (WDR12) were identified as the hub genes, and the three hub genes were up-regulated in the chondrosarcoma. Chondrosarcoma patients with high expression levels of DDX10 (Logrank P = .0052; HR (high) = 1.8; n (high) = 131, 50%), and BYSL (P = 6.5e-05; HR (high) = 2.3; n (high) = 131, 50%) had poorer overall survival times than those with low expression levels.DDX10 and BYSL genes may provide reliable molecular markers and effective therapeutic targets for chondrosarcoma and glioma.
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We applied GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r), an online tool based on GEO query and limma R packages, to identify DEGs between esophagus cancer and normal group.
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We applied GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r), an online tool based on GEO query and limma R packages, to identify DEGs between esophagus cancer and normal group.
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The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
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Using GEO2R to analyze GSE29745 and GSE48420 downloaded from GEO, the study identified 1442 DEGs shared by the two datasets.
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Gene Set Enrichment (GSE) 29745 and GSE48420 were downloaded from the Gene Expression Omnibus (GEO) database.
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Differently expressed genes (DEGs) were identified by the GEO2R.
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The Venn diagram revealed 1442 DEGs shared by the two datasets (Fig. 2).
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Lost miRNA surveillance of NOTCH, IGFR pathway-road to sarcomagenesis
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Differently expressed genes (DEGs) were identified by the GEO2R. We annotated the function of common DEGs through Digital Audio/Video Interactive Decoder (DAVID) and Metascape. Protein-protein interaction network construction was performed through STRING. Hub genes were identified by the two different algorithms (MCC, EPC). DDX10 and BYSL were key factors in embryo implantation and development, and plays a role in a variety of cancers. The role of the DDX10 and BYSL on the glioma derived from the chondrosarcoma would be explored by the clinical samples.A total of 1442 DEGs were identified. The variations in DEGs were mainly enriched in vasculature development, cell motion, blood vessel development, cell migration, regulation of cell proliferation, regulation of cell proliferation, wound healing, biological adhesion, growth factor binding, identical pathways in cancer, and p53 signaling pathway. 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