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

Crosstalk between gap junction intracellular communication (GJIC), 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 duanyu18135 only in the presence of the GJIC inducer, cAMP. Nuclear duanyu18135 levels were not detectable. By contrast, cells on EHS-drip expressed β-casein in a manner and nuclear duanyu18135 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 duanyu18135 nuclear translocation.

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