Gap junctions mediate STAT5-independent β-casein expression in CID-9 mammary epithelial cells

Rabih S. Talhouk*, Antoine A. Khalil, Rachid Bajjani, Gilbert J. Rahme, Marwan E. El-Sabban

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Crosstalk between gap junction intracellular communication (GJIC), STAT5 and OCT-1 in gap junction (GJ)-dependent β-casein expression was investigated. CID-9 mammary cells plated with prolactin on non-adherent substratum (poly-HEMA) expressed β-casein independent of STAT5 only in the presence of the GJIC inducer, cAMP. Nuclear STAT5 levels were not detectable. By contrast, cells on EHS-drip expressed β-casein in a STAT5-dependent manner and nuclear STAT5 levels were up-regulated. A 75 kDa OCT-1 isoform was detected in conditions that induced β-casein expression regardless of substratum. Interestingly, 40 and 28 kDa OCT-1 isoforms were induced in cells on polyHEMA with cAMP. Electrophoretic mobility shift assays (EMSA) for OCT-1 revealed two band shifts in cells on polyHEMA with cAMP and on EHS-drip, which were repressed by the GJIC inhibitor, 18α-GA. These studies demonstrated that mammary cells on polyHEMA expressed β-casein in response to prolactin in a pathway that involves GJIC and OCT-1 and is independent of STAT5 nuclear translocation.

Original languageEnglish
Pages (from-to)104-116
Number of pages13
JournalCell Communication and Adhesion
Volume18
Issue number5
DOIs
Publication statusPublished - Oct 2011
Externally publishedYes

Keywords

  • β-casein
  • GJIC
  • OCT-1
  • STAT5

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