ABSTRACT

Colorectal cancer (CRC) continues to pose obstacles for treatment; however, a deeper comprehension of the driving epigenetic modifications can help develop new therapeutics. Previous studies have shown correlations between DNA methylation and CRC, increasing the need to identify potential causative methylation events. We hypothesized that the promoter of the DKK3 gene in HCT116 colorectal cancer cells is a differentially hypermethylated region (DMR). Decreased cell growth following treatment with the methyl-transferase inhibitor, decitabine, prompted us to study the role of DNA methylation and CRC at the molecular level. In this study, methylation of the DKK3 gene promoter between decitabine and DMSO-treated cells was studied through bisulfite sequencing. Methylation quantification following bisulfite sequencing revealed significant reduction of methylation by decitabine (~41%) in the analyzed CpG sites, suggesting the DKK3 promoter is differentially methylated in HCT116 cells. In the future, we hope to replicate this data, as well as see if artificially expressing DKK3 slows CRC cell growth. In conjunction with a deeper look into the role of chromatin structure and histone modifications in the DKK3 region, we hope to come closer in identifying the causal methylation events of CRC.

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