Abstract
Colorectal cancer (CRC) is one of the most common and serious types of malignancy worldwide. The embryonic ectoderm development (EED) gene is important to maintain transcriptional repressive states of genes over successive cell generations. The present study aimed to investigate the association between EED methylation and CRC. A total of 111 CRC tissue samples, 111 paired para-tumor tissues and 20 colorectal normal tissues were obtained for EED methylation assay, which was performed using a quantitative methylation-specific polymerase chain reaction. The percentage of methylated reference was calculated to represent the DNA methylation level. A dual-luciferase reporter gene assay was used to detect the gene promoter activity of a EED fragment. The current results revealed a significant difference in the EED methylation levels among tumor, para-tumor and normal colorectal tissues (tumor vs. para-tumor vs. normal, 5.03±4.61 vs. 8.65±11.50 vs. 40.12±45.31; F=45.014; P<0.0001). The dual-luciferase reporter gene assay demonstrated that the transcriptional activity of recombinant pGL3-EED plasmid was significantly higher compared with that of the pGL3-Basic control vector (fold-change, 3.15; P=0.014), which suggests the EED fragment can promote gene expression. In conclusion, the present study demonstrated that EED hypomethylation may be an important factor associated with CRC.