Figure 4: Identification of DCLK3-associated gene sets and clinical parameters in the SYSCOL RNA-seq cohort. | Nature Communications

Figure 4: Identification of DCLK3-associated gene sets and clinical parameters in the SYSCOL RNA-seq cohort.

From: The non-coding variant rs1800734 enhances DCLK3 expression through long-range interaction and promotes colorectal cancer progression

Figure 4

(a) GSEA analysis revealed DCLK3 correlated cancer hallmark gene sets. EMT and oxidative phosphorylation-associated gene sets were highly significantly associated with the DCLK3 expression in both healthy and tumour tissues. In addition, some DCLK3-associated gene sets showed healthy or tumour tissue specificity (P-values were calculated in GSEA based on Pearson’s correlation). The expression of key EMT markers showed good correlation with the DCLK3 expression. (b) The DCLK3 expression was preferentially elevated in the tumours and especially the malignant tissues. However, we did not observe a clear difference between MSI and MSS tumours (P-values: Mann–whitney U-test (MW test) and Kruskal–Wallis test (KW test)). (c) A proposed model describing how rs1800734 modifies the risk of CRC malignancy. TFAP4 and ETS family members specifically bind to the protective G- or risk A-allele, respectively. The rs1800734-ETS interaction increases the enhancer activity of the rs1800734 locus and enhances the expression of DCLK3 through an increased chromatin interaction. Cancer cells with the elevated DCLK3 expression undergo EMT and therefore metastasize to distal sites.

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