Incomplete ablation of colon cancer cells may induce activation of dormant cells: Evidence from bioinformatics analysis.

PURPOSE

It is not yet verified whether incomplete radiofrequency ablation (iRFA) induces tumor progression and hypoxia related to tumor dormancy. This study showed the relationship between iRFA and tumor dormancy.

MATERIALS AND METHODS

To identify the candidate genes in the control and iRFA-treated colon cancer cells, microarray datasets GSE138224 were downloaded from Gene Expression Omnibus database. Using NetworkAnalyst, the differentially expressed genes (DEGs) were identified, function enrichment analyses were performed, and the protein-protein interaction (PPI) network and key PPI network were constructed.

RESULTS

A total of 656 DEGs were identified, comprising 637 downregulated and 19 upregulated genes. The enriched functions and pathways of the upregulated DEGs include an immune effector process, regulation of tyrosine phosphorylation of signal transducer and activator of transcription (STAT) protein, tyrosine phosphorylation of STAT protein, JAK-STAT cascade, and regulating JAK-STAT cascade, and CCL5 gene participated in regulating the JAK-STAT signaling pathway. The downregulated DEGs were mainly enriched in extracellular matrix-receptor interaction, PI3K-Akt signaling, Wnt signaling, transforming growth factor-beta signaling, and mitogen-activated protein kinase signaling pathways. There are three key PPI networks of DEGs (degree ≥10 and hub genes >3). The dormancy-related genes Bmp4 and Ccl5 were regarded as hub genes in the PPI network with Bmp4 as a downregulated gene and CCL5 as an upregulated gene.

CONCLUSION

The identified DEGs and function enrichment analyses in this study aid the understanding of molecular mechanisms underlying the relationship between iRFA and tumor dormancy.