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Gene expression profile and bioinformatics analysis revealed key molecular characteristics of chordoma-before and
Guoyong Xu1, Chong Liu1,2, Tuo Liang1
1Guangxi Medical University.
Background:
Chordoma is a rare malignant tumor with limited treatment. Recent studies have shown that the proliferation and invasion ability of chordoma after Tumor necrosis factor alpha (TNF-α) treatment is enhanced, which may activate the gene pathway involved in the development of chordoma. This study tends to identify differentially expressed genes (DEGs) before and after treatment of TNF-α in chordoma cell line, providing a new target for future molecular therapy of chordoma.
Methods:
The gene expression profile of GSE101867 was downloaded from the Gene Expression Omnibus database, and the differentially expressed genes were obtained using GEO2R. Based on the CLUEGO plugin in Cytoscape, DEGs functionality and enrichment analysis. A protein-protein interaction (PPI) network was constructed using Cytoscape based on data collected from the STRING online dataset. The Hub genes are selected from the CytoHubba, the first 20 genes that coexist with the KEGG tumor-related pathway.
Results:
A total of 560 genes, including 304 up-regulated genes and 256 down-regulated genes, were selected as DEGs. Obviously, GO analysis shows that up-regulated and down-regulated DEGs are mainly enriched in biological processes such as synaptic tissue, cell adhesion, extracellular matrix organization and skeletal system development. DEGs are mainly enriched in tumor-associated pathways such as Pi3k-akt Signal path, Rap1 signal path. Three key genes were identified: PDGFRB, KDR, FGF2. All of these genes are involved in the tumor-associated pathways described previously.
Conclusion:
This study is helpful in understanding the molecular characteristics of chordoma development. Hub genes PDGFRB, KDR, FGF2 and pi3k-akt signaling pathway, Rap1 signaling pathway will become a new target for the future treatment of chordoma.
Insights
Tumor Necrosis Factor alpha (TNF-α) treatment enhances chordoma cell proliferation. Key genes PDGFRB, KDR, FGF2 and associated pathways offer new therapeutic targets for this rare cancer.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Chordoma is a rare malignant tumor with limited therapeutic options.
- Tumor Necrosis Factor alpha (TNF-α) treatment can paradoxically enhance chordoma cell proliferation and invasion.
- Identifying molecular pathways activated by TNF-α is crucial for developing new chordoma treatments.
Purpose of the Study:
- To identify differentially expressed genes (DEGs) in chordoma cells before and after TNF-α treatment.
- To elucidate the molecular mechanisms underlying TNF-α-induced chordoma progression.
- To discover novel molecular targets for chordoma therapy.
Main Methods:
- Gene expression profiling data (GSE101867) was analyzed using GEO2R.
- Functional and enrichment analysis of DEGs was performed using Cytoscape and CLUEGO.
- Protein-protein interaction (PPI) network construction and hub gene identification were conducted using STRING and CytoHubba.
Main Results:
- A total of 560 DEGs (304 up-regulated, 256 down-regulated) were identified.
- DEGs were enriched in biological processes including cell adhesion and skeletal system development.
- Key genes PDGFRB, KDR, and FGF2 were identified within tumor-associated pathways like Pi3k-akt and Rap1 signaling.
Conclusions:
- The study provides insights into the molecular characteristics of chordoma development.
- Hub genes PDGFRB, KDR, FGF2, and the Pi3k-akt and Rap1 signaling pathways represent potential therapeutic targets for chordoma.
- These findings pave the way for future molecular therapies against chordoma.
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