The expression of the tumor suppressor gene connexin 26 is not mediated by methylation in human esophageal cancer cells

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Abstract
Gap junctional intercellular communication is thought to play an important role in cell differentiation and tissue homeostasis. Gap junctional intercellular communication is mediated by intercellular channels connecting adjacent cells and composed of connexin (Cx) proteins. Until now, approximately 20 different Cx have been characterized in mammals, and they are expressed in a tissue‐specific manner. The downregulation of Cx expression is often observed in tumors and transformed cell lines and is believed to contribute to the loss of proliferating control. Connexin 26 (Cx26) is a Cx constitutively expressed in the normal epithelial esophageal tissue. In the majority of esophageal tumors, Cx26 expression is low or totally absent. CpG island hypermethylation is known to be associated with gene silencing in cancer. Because the promoter and exon 1 region of Cx26 are rich in CpG dinucleotides, we examined whether the loss of Cx26 expression in human esophageal TE cell lines was related to the hypermethylation of this region. We analyzed several TE cell lines derived from different human esophageal carcinomas and exhibiting different levels of Cx26 expression by using methylation‐sensitive restriction digestion and Southern blot analysis. We did not find any correlation between the Cx26 expression and the methylation level of the promoter region of the Cx26 gene. Our results suggest that methylation was probably not involved as a primary mechanism of Cx26 regulation in human esophageal cancer cell lines.