By combination analysis of the methylation array data and expression data, we found 13 hypermethylated CpG sites in the promoter region of EPB41L3 and a greater than ten fold change in down-regulation upon comparison between tumor tissues and normal tissues. This result suggests in ESCC the expression of EBP41L3 is decreased due to its promoter methylation, which is Navitoclax consistent with the previous studies in other types of tumors. Glutathione peroxidase 3 catalyzes the reduction of peroxides at the expense of glutathione and protects cells against oxidative damage. Thus, the silencing of GPX3 may impair defenses against endogenous and exogenous genotoxic compounds, which could increase gene mutation rates. GPX3 has been found to be frequently hypermethylated in prostate cancer, esophageal adenocarcinoma, and gastric cancer. Furthermore, the promoter hypermethylation of GPX3 was correlated with the down-regulation of mRNA and/or protein expression. In addition, the mRNA expression can be restored by demethylated agents. Moreover, suppressive activity of tumor growth and metastasis was demonstrated by both in vitro and in vivo studies. Our result showed that the methylation frequency in tumor tissues is 54.8%, which is significantly higher than 9.5% in paired adjacent normal surrounding tissues. This result is consistent with a previous study that found that the methylation of GPX3 promoter was more frequent in ESCC tumor tissues than in adjacent nontumor tissues . In addition, we analyzed the correlation of the methylation of GPX3 promoter and clinico-parameter of the patients. We found that the frequency of methylation is higher in pT3 patients and pN2 patients compared with pT1-T2 and pN0-N1 patients. These results suggest that the methylation of GPX3 may be involved in the progression and lymphnoid metastais in ESCC. COL14A1 is a large extracellular matrix glycoprotein associated with mature collagen fibrils. Alterations in extracellular matrix composition have been implicated in tumor progression and metastasis. COL14A1 interacts with decorin, a small leucinerich proteoglycan, which has incrementally been shown to be a powerful inhibitor of growth in a wide variety of tumor cells. This effect is specifically mediated by the interaction of decorin core protein with the epidermal growth factor receptor and other ErbB family proteins. Previous studies have shown that aberrant COL14A1 DNA methylation has been tested in renal cancer cell lines and primary renal cancers, and the methylation correlated with silencing or down-regulating of mRNA expression. Moreover, RNAi-induced reduced expression of COL14A1 resulted in the growth of renal cancer cells in vitro. In our study, we observed that the methylation frequency of COL14A1 was significantly higher in tumor tissues than that in adjacent normal surrounding tissues. We found that the moderate pathologically differentiated samples have a higher methylation frequency of COL14A1, compared with well or poor pathologically differentiated samples.