Cluster analysis of DMRs and corresponding pathway analysis. Analysis of DMRs and methylation-based pathway analysis integrating RNA expression data between clusters. Cluster 1 compared with cluster 2 and cluster 3 (A), cluster 2 compared with cluster 1 and cluster 3 (B), and cluster 3 compared with cluster 1 and cluster 2 (C). DMR statistical analysis was conducted using the Pearson χ2 analysis comparing expected with observed values to determine P value. AKT, protein kinase B; CDK, cyclin-dependent kinase; ECM, extracellular matrix; ERK, extracellular signal-regulated kinase; FAK, focal adhesion kinase; GPCR, G protein-coupled receptors; ID1, inhibitor of DNA binding 1; IGF-1, insulin-like growth factor 1; mTOR, mammalian target of rapamycin; PTEN, phosphatase and tensin homolog; TGF, transforming growth factor; TME, tumor microenvironment; VEGF, vascular endothelial growth factor.
Figure 2.

Cluster analysis of DMRs and corresponding pathway analysis. Analysis of DMRs and methylation-based pathway analysis integrating RNA expression data between clusters. Cluster 1 compared with cluster 2 and cluster 3 (A), cluster 2 compared with cluster 1 and cluster 3 (B), and cluster 3 compared with cluster 1 and cluster 2 (C). DMR statistical analysis was conducted using the Pearson χ2 analysis comparing expected with observed values to determine P value. AKT, protein kinase B; CDK, cyclin-dependent kinase; ECM, extracellular matrix; ERK, extracellular signal-regulated kinase; FAK, focal adhesion kinase; GPCR, G protein-coupled receptors; ID1, inhibitor of DNA binding 1; IGF-1, insulin-like growth factor 1; mTOR, mammalian target of rapamycin; PTEN, phosphatase and tensin homolog; TGF, transforming growth factor; TME, tumor microenvironment; VEGF, vascular endothelial growth factor.

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