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Published on: October 4, 2019
Transcriptome and coexpression network analysis of the human glioma cell line Hs683 exposed to candoxin
1Department of Neurosurgery, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Objective:
Gliomas are the most common primary tumours of the central nervous system. Snake venom, such as candoxin (CDX) isolated from Bungarus candidus, inhibits glioma cell proliferation. This study explored the gene regulation profile of CDX-treated human glioma Hs683 cells.
Methods:
Using microarray technology and bioinformatics analyses the underlying molecular mechanism of action of CDX was evaluated by constructing gene regulation and protein-protein interaction co expression networks.
Results:
CDX treatment induced a large number of related genes at the transcriptional level. The MYC gene (v-myc myelocytomatosis viral oncogene homologue [avian]) had a key role in the response of Hs683 cells to CDX treatment. Activation of MYC upregulated NDRG1 (N-myc downstream regulated 1), WNT10B (wingless-type mouse mammary tumour virus integration site family, member 10B), CASP9 (caspase 9, apoptosis-related cysteine peptidase) and CDKN2A (cyclin-dependent kinase inhibitor 2A), and downregulated ID3 (inhibitor of DNA binding 3, dominant negative helix-loop-helix protein) and SLC1A4 (solute carrier family 1 [glutamate/neutral amino acid transporter], member 4). In addition, a subnetwork was constructed among SPP1 (secreted phosphoprotein 1), SDC1 (syndecan 1) and CD44 based on protein-protein interactions, and these genes were predicted to be involved in glioma cell invasion.
Conclusion:
These findings might provide novel therapeutic targets for glioma chemotherapy.
Insights
Candoxin (CDX) from snake venom inhibits glioma cell growth. CDX alters gene expression in human glioma cells, highlighting MYC as a key regulator and suggesting new therapeutic targets for glioma.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Toxicology
Background:
- Gliomas are primary central nervous system tumors.
- Snake venom component candoxin (CDX) inhibits glioma cell proliferation.
- Understanding CDX's molecular mechanism is crucial for therapeutic development.
Purpose of the Study:
- To investigate the gene regulation profile of CDX-treated human glioma Hs683 cells.
- To elucidate the molecular mechanisms underlying CDX's anti-glioma effects.
- To identify potential therapeutic targets for glioma treatment.
Main Methods:
- Microarray technology was employed to analyze gene expression changes.
- Bioinformatics analyses were used to construct gene regulation and protein-protein interaction networks.
- Co-expression network analysis identified key regulatory genes and pathways.
Main Results:
- CDX treatment significantly altered gene expression at the transcriptional level.
- The MYC gene was identified as a key regulator in Hs683 cells' response to CDX.
- CDX modulated the expression of genes involved in cell proliferation, apoptosis, and invasion, including NDRG1, WNT10B, CASP9, CDKN2A, ID3, and SLC1A4. A subnetwork involving SPP1, SDC1, and CD44 was implicated in glioma cell invasion.
Conclusions:
- CDX significantly impacts glioma cell gene regulation.
- MYC activation plays a critical role in CDX's anti-glioma activity.
- The identified genes and pathways represent potential novel therapeutic targets for glioma chemotherapy.
