Academics

Colon cancer is one of the most prominent cancer types in the world, being in second place as the leading cause of cancer death. Even though the molecular mechanisms underlying this disease are not yet understood, epigenetic modifications have been attributed to possible involvement in tumorigenesis. In particular, DNA methylation is frequently seen across multiple cancer patients. There are high-confidence differentially methylated regions (DMRs) that could provide insight into this modification and its role in cell survival and proliferation. In this study, the researchers use the HCT-116 colorectal cancer cell line as a model to study the effects of treatment with the demethylating anti-cancer drug, decitabine, on the methylation sites of the SOX21 DMR. For this, decitabine effects on cell growth and demethylation were analyzed by global demethylation assay using methylation-sensitive restriction enzyme HpaII. Followed by bisulfite PCR Sanger sequencing analysis to quantify CpG methylation for HCT116 cells and after treatment. It was found that decitabine is a good agent for demethylating DNA and inhibiting cell growth. As of SOX21 DMR, it appeared that it was originally unmethylated, and thus, decitabine partially demethylated specific CpG sites at the promoter region. The data was uploaded to the UCSC genome browser and compared with previous ENCODE Project data, which indicated new CpG sites near known methylated sites for SOX21 DMR. For future research, the researchers aim to investigate chromatin accessibility along with methylation sites to investigate gene expression and possible mechanisms involved in colon cancer tumorigenesis, expanding site-specific understanding of this DMR. 

Read the full article here.