Dataset Information

Recognition of Key Genes in Human Anaplastic Thyroid Cancer via the Weighing Gene Coexpression Network.

ABSTRACT:

Methods

For determining pathways and key genes that have relation with development of ATC, differentially expressed genes (DEGs) from GSE33630 as well as GSE65144 expression microarray were screened. Furthermore, we also worked on carrying out the task of constructing a protein-protein interaction (PPI) network and the work of weighing gene coexpression network (WGCNA). DAVID was utilized for the performance of the Gene Ontology (GO) as well as KEGG pathway enrichment analyses for DEGs. We used TCGA THCA data and GSE53072 to further verify the hub gene and hub pathway.

Results

We came to the conclusion of the recognition of a total of 1063 genes as DEGs. Analysis regarding functional and pathway enrichment showed that there existed a notable enrichment of upregulated DEGs in the organization of extracellular structure and matrix organization, as well as in organelle fission and nuclear division. The downregulated DEG was markedly gathered in the thyroid hormone metabolic process and generation, as well as in the metabolic process of cellular modified amino acid. We identified 10 hub genes (CXCL8, CDH1, AURKA, CCNA2, FN1, CDK1, ITGAM, CDC20, MMP9, and KIF11) through the PPI network, which might be strongly linked to the carcinogenesis and the development of ATC. In the coexpression network, 6 modules that were relevant to ATC were recognized. The modules were related to the interaction of signaling pathway of p53, Hippo, PI3K/Akt, and ECM-receptor. This hub genes and hub pathway were further successfully validated as a potential biomarker for carcinogenesis and prediction in another database GSE53072.

Conclusion

To summarize, this research displayed an illustration of hub genes and pathways that had relation with ATC development, which suggested that DEGs and hub genes, recognized on the basis of bioinformatics analyses, were valuable in the diagnosis for patients with ATC.

SUBMITTER: Gong Y

PROVIDER: S-EPMC9247818 | biostudies-literature |

REPOSITORIES: biostudies-literature

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