Modulation of the connexin26 tumor suppressor gene expression through methylation in human mammary epithelial cell lines

Rakesh Singal, Z. J. Tu, J. M. Vanwert, G. D. Ginder, D. T. Kiang

Research output: Contribution to journalArticle

38 Scopus citations


Background. Normal mammary epithelial cells express mainly gap junction connexin 26 (Cx26) that is either reduced or absent in breast cancers. Since connexin gene mutations are rare we examined if Cx26 gene repression is related to hypermethylation. Materials and Methods. Five breast epithelial cell lines were examined for Cx26 mRNA expression and hypermethylation. Treatment with a DNA methyltransferase inhibitor, 5-Aza-2'-deoxycytidine (5-Aza-CdR) was carried out to determine if Cx26 gene expression could be upregulated. Results. Cx26 expression was easily detectable in an immortalized human mammary epithelial cell line (MCF-10) and markedly diminished (MDA-MB231) or undetectable in (MCF-7, BT-20, T47-D) breast cancer cell lines. Hypermethylation of the Cx26 5' region was observed in MCF-10 and MCF-7 cells. Treatment with 5-Aza-CdR resulted in slight or no induction in Cx26 expression in breast cancer cell lines. Conclusions. Hypermethylation is unlikely to be a major mechanism for Cx26 gene repression in human mammary cancer cell lines.

Original languageEnglish
Pages (from-to)59-64
Number of pages6
JournalAnticancer Research
Issue number1 A
StatePublished - Apr 18 2000
Externally publishedYes



  • Breast cancer
  • Connexin 26 gene
  • DNA methylation
  • Gene expression

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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