CCL26 silence represses colon cancer by inhibiting the EMT signaling pathway

This study aimed to determine the expression and investigate the role of chemokine 26 (CCL26) in colon cancer cells. The Cancer Genome Atlas (TCGA) analysis, qRT-PCR, and western blotting were used to detect CCL26 expression while the Kaplan-Meier plotter was used to analyze the survival of patients with colon cancer. Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, and Transwell assays were performed to measure the viability, proliferation, apoptosis, and migration and invasion of colon cancer cells, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to analyze the signaling pathways regulated by CCL26. Western blotting, used to measure protein expression in this study, found overexpression of CCL26 in colon tumors. Low CCL26 levels were associated with better survival of patients as CCL26 siRNAs markedly reduced viability and proliferation, accelerated apoptosis, decreased migration and invasion, enhanced E-cadherin expression, and reduced N-cadherin and vimentin expression in cancer cells. The opposite results were obtained in CCL26-overexpressed colon cancer cells. In addition, CCL26 activated the epithelial-mesenchymal transition (EMT) pathway. CCL26 siRNAs suppressed the expression of tissue inhibitor matrix metalloproteinase 1 (TIMP1), nicotinamide N-methyltransferase (NNMT), and fibromodulin (FMOD), while CCL26 overexpression significantly increased the expression of all. EMT inhibition using the EMT inhibitor C19 eliminated the effect of CCL26 overexpression on colon cancer cells. In summary, CCL26 is involved in colon cancer progression through regulation of the EMT signaling pathway.