WT1 Inhibits Human Renal Carcinoma Cell Proliferation and Induces G2/M Arrest by Upregulating IL-24 Expression

Figure 6

Genome-wide WT1 association in renal cancer cells. (a) Table showing data and flow of analysis of the ChIP-Seq experiment from sequence reads to annotated gene assignment of the WT1-binding sites. (b) Analysis of the motifs associated with WT1 peaks showed enrichment for known WT1-binding sequences. (c) Distribution of WT1-binding regions in the renal cancer cell genome. (d) Distribution of WT1 promoter peaks relative to the TSS. (e) WT1-binding motifs identified by ChIP-Seq analysis. (f–i) Significantly enriched GO annotations and KEGG pathways of WT1-related genes analyzed by DAVID. (f) Biological processes, (g) molecular functions, (h) cellular components, and (i) KEGG pathway analysis. (j) The expression level of WT1-target genes was verified in WT1-overexpressing cells by RT-qPCR. Experiments were conducted in triplicate (); error bars represent standard errors; .

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