Related Experiment Video
Updated: Dec 20, 2025
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
Published on: July 22, 2020
Identification of Hub Genes in Atypical Teratoid/Rhabdoid Tumor by Bioinformatics Analyses
1Department of Neurosurgery, Yuquan Hospital, School of Clinical Medicine, Tsinghua University, Beijing, 100040, China.
Abstract:
Atypical teratoid/rhabdoid tumor (ATRT) is a devastating intracranial tumor in children. Currently, its molecular mechanisms cannot be studied effectively because patient samples are limited, and many factors are involved in its pathogenesis. In this study, we analyzed three gene expression profile data sets obtained from the Gene Expression Omnibus (GEO) database to identify genes that participate in ATRT. The datasets were integrated and analyzed using the RobustRankAggreg method to screen for differentially expressed genes (DEGs). We identified 197 DEGs, including 94 downregulated and 103 upregulated genes which were then used for gene set enrichment analysis. The results showed that the downregulated genes were mainly enriched in synaptic vesicle cycle, nicotine addiction, and GABAergic synapse, whereas the upregulated genes were enriched in the cell cycle, p53 signaling pathway, and cellular senescence. Consistent with these results, gene set enrichment analysis showed that E2F targets, G2M checkpoints, and MYC targets were significantly enriched in datasets. Protein-protein interaction (PPI) network revealed that CDK1, CCNA2, BUB1B, CDC20, KIF11, KIF20A, KIF2C, NCAPG, NDC80, NUSAP1, PBK, RRM2, TPX2, TOP2A, and TTK were hub genes. NetworkAnalyst algorithm was used to predict the transcription factor (TF), and the results showed that MYC, SOX2, and KDM5B could regulate these hub genes. In conclusion, the present study brings a new perspective of ATRT pathogenesis and the strategy targeted to cell cycle related gene may be promising treatments for the disease.
Insights
This study identifies key genes involved in atypical teratoid/rhabdoid tumor (ATRT) pathogenesis by analyzing gene expression data. Targeting cell cycle-related genes shows promise for treating this pediatric brain tumor.
Area of Science:
- Pediatric Oncology
- Molecular Biology
- Genomics
Background:
- Atypical teratoid/rhabdoid tumor (ATRT) is a severe pediatric brain tumor with poorly understood molecular mechanisms due to limited patient samples.
- Identifying key molecular players is crucial for understanding ATRT pathogenesis and developing targeted therapies.
Purpose of the Study:
- To identify differentially expressed genes (DEGs) and key molecular pathways implicated in ATRT pathogenesis.
- To uncover potential therapeutic targets by analyzing gene expression profiles from publicly available datasets.
Main Methods:
- Integrated analysis of three gene expression profile datasets from the Gene Expression Omnibus (GEO) database using RobustRankAggreg.
- Performed gene set enrichment analysis (GSEA) and constructed a protein-protein interaction (PPI) network.
- Utilized NetworkAnalyst to predict regulatory transcription factors (TFs).
Main Results:
- Identified 197 DEGs (94 downregulated, 103 upregulated) in ATRT.
- Downregulated genes enriched in synaptic functions; upregulated genes in cell cycle, p53 signaling, and senescence pathways.
- Key upregulated pathways included E2F targets, G2M checkpoints, and MYC targets. Identified 15 hub genes and potential TFs (MYC, SOX2, KDM5B).
Conclusions:
- This study provides novel insights into ATRT pathogenesis, highlighting the critical role of cell cycle regulation.
- Targeting cell cycle-related genes presents a promising therapeutic strategy for ATRT.
More Related Videos
09:40Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
09:37Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
