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Updated: Oct 4, 2025
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
Key genes involved in cell cycle arrest and DNA damage repair identified in anaplastic thyroid carcinoma using
Zhi Zhang1, Zhenning Zou2, Haixia Dai3
1Department of Thyroid and Mammary Vascular Surgery, the Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Background:
Since anaplastic thyroid carcinoma (ATC) has rapid progression and a poor outcome, identification of the key genes and underlying mechanisms of ATC is required.
Methods:
Gene expression profiles of GSE29265 and GSE33630 were available from the Gene Expression Omnibus database. The two profile datasets included 19 ATC tissues, 55 normal thyroid tissues and 59 papillary thyroid cancer (PTC) tissues. Differentially expressed genes (DEGs) between ATC tissues and normal thyroid tissues as well as ATC tissues and PTC tissues were identified using the GEO2R tool. Common DEGs between the two datasets were selected via Venn software online. Then, we applied the Database for Annotation, Visualization and Integrated Discovery for Kyoto Encyclopedia of Gene and Genome pathway and gene ontology (GO) analyses. Additionally, protein-protein interactions (PPIs) of these DEGs were visualized via Cytoscape with Search Tool for the Retrieval of Interacting Genes. In the PPI networks analyzed by the Molecular Complex Detection plug-in, all 54 upregulated core genes were selected. Furthermore, Kaplan-Meier analysis was applied to analyze overall survival based on these 54 genes. Then, we used the DrugBank database to identify drug relationships for the 54 genes. Additionally, we validated the correlations between genes enriched in pathways and genes identified as prognosis biomarkers of THCA by Gene Expression Profiling Interactive Analysis.
Results:
Four genes (CCNB1, CCNB2, CDK1 and CHEK1) involved cell cycle arrest and DNA repair were significantly enriched in the G2/M phase of the cell cycle pathway and before G2 phase arrest of the P53 pathway. Inhibitors of CHEK1, CDK1 and TOP2A were identified in the DrugBank database. ANLN, DEPDC1, KIF2C, CENPN, TACC3 CCNB2 and CDC6 were hypothesized to be prognostic biomarkers of ATC. Furthermore, CCNB1, CCNB2, CDK1 and CHEK1 were significantly positively associated with these prognosis genes.
Conclusions:
CCNB1, CCNB2, CDK1 and CHEK1 may be key genes involved cell cycle arrest and DNA damage repair in ATC. Further studies are required to confirm the contributions of the identified genes to ATC progression and survival.
Insights
Key genes CCNB1, CCNB2, CDK1, and CHEK1 are implicated in cell cycle arrest and DNA repair in anaplastic thyroid carcinoma (ATC). These findings may offer new therapeutic targets for this aggressive cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Anaplastic thyroid carcinoma (ATC) is characterized by rapid progression and poor patient outcomes.
- Identifying key genes and molecular mechanisms driving ATC is crucial for developing effective treatments.
Purpose of the Study:
- To identify key genes and pathways involved in the development and progression of anaplastic thyroid carcinoma (ATC).
- To explore potential therapeutic targets and prognostic biomarkers for ATC.
Main Methods:
- Analysis of gene expression profiles from public databases (GSE29265, GSE33630) comparing ATC, normal thyroid, and papillary thyroid cancer (PTC) tissues.
- Identification of differentially expressed genes (DEGs), pathway and gene ontology (GO) analyses, and protein-protein interaction (PPI) network construction.
- Kaplan-Meier survival analysis and drug target identification using the DrugBank database.
Main Results:
- Four genes (CCNB1, CCNB2, CDK1, CHEK1) were significantly enriched in cell cycle pathways (G2/M phase) and the P53 pathway, indicating roles in cell cycle arrest and DNA repair.
- Several genes, including ANLN, DEPDC1, KIF2C, CENPN, TACC3, CCNB2, and CDC6, were identified as potential prognostic biomarkers for ATC.
- CCNB1, CCNB2, CDK1, and CHEK1 showed a significant positive association with these prognostic genes.
Conclusions:
- CCNB1, CCNB2, CDK1, and CHEK1 are likely key genes involved in cell cycle arrest and DNA damage repair in ATC.
- These identified genes represent potential therapeutic targets for managing ATC progression and improving patient survival.
- Further research is necessary to validate the precise roles of these genes in ATC pathogenesis and clinical outcomes.
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