Epigenetic inactivation of deleted in lung and esophageal cancer 1 gene by promoter methylation in gastric and colorectal adenocarcinoma.

Deleted in Lung and Esophageal Cancer 1 (DLEC1) gene was a new candidate tumor suppressor gene, we evaluated the diagnostic role of DLEC1 methylation in gastric adenocarcinoma (GAC) and colorectal adenocarcinoma (CRAC). Methylation-specific polymerase chain reaction (MSP) was used to determine the promoter methylation status of DLEC1 gene in tissue and serum DNA. DLEC1 gene expression was determined by immunohistochemistry. DLEC1 methylation was detected in 38.5% (25/65) of GAC and 45.1% (32/71) of CRAC tissues, while seldom in the adjacent normal tissues of stomach (8.0%, 4/50) and colorectum (7.1%, 4/56) (p < 0.001). The hypermethylation status of DLEC1 was associated with low or absent of DLEC1 protein expression both in tumor and pre-malignant lesions (p < 0.001), but not correlated with patients' clinicopathological features and elevated CEA/CA19-9 levels. Moreover, 33.8% (22/65) of GAC and 39.4% (28/71) of CRAC serums had DLEC1 methylation, which was higher than that in the serums of cancer-free controls (p < 0.001), and the concordance of DLEC1 methylation in tumor tissues and corresponding serum samples was well. Epigenetic inactivation of DLEC1 was crucial in gastric and colorectal carcinogenesis. DLEC1 methylation in serum may be a promise biomarker for GAC and CRAC early diagnosis.