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Fig. 6 | Clinical Epigenetics

Fig. 6

From: Transcriptomic profiling disclosed the role of DNA methylation and histone modifications in tumor-infiltrating myeloid-derived suppressor cell subsets in colorectal cancer

Fig. 6

Differential gene expression and functional network analyses of APCs, PMN-MDSCs, and I-MDSCs in CRC microenvironment. Hierarchical clustering of APCs and I-MDSCs from two TTs (patients #07 and #08) on differentially expressed RNA transcripts from RNA-Seq data (a). Heat maps show the TPM representing fold change relative to the mean expression of WNT signaling, SNARE signaling, and JNK pathway activation in I-MDSCs, compared with APCs (b). Hierarchical clustering of PMN-MDSCs and I-MDSCs from two TTs on differentially expressed RNA transcripts from RNA-Seq data (c). Heat maps show the TPM representing fold change relative to the mean expression of colorectal cancer-, binding of HDAC-, cell migration-, NFκB-, and IL-1β production-related genes in PMN-MDSCs, compared with APCs (d). Hierarchical clustering of PMN-MDSCs and I-MDSCs from two TTs on differentially expressed RNA transcripts from RNA-Seq data (e). Heat map shows the TPM representing fold change relative to the mean expression of tumor progression-, migration and metastasis-, and DNA methylation-related genes in PMN-MDSCs, compared with I-MDSCs (f). Heat map shows the TPM representing fold change relative to the mean expression of genes associated with transcriptional regulation and signal transduction genes in PMN-MDSCs, compared with I-MDSCs (g). The mRNA expression levels for selected genes in tumor-infiltrating sorted myeloid cells, PMN-MDSCs vs. APCs were validated by RT-PCR (h). The relative gene expression was normalized to β-actin. Results obtained from six CRC patients, #05, #07, #08, #09, #44, and #53, and expressed as mean ± SEM. N.D. not detected

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