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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Organization of mammary epithelial cells into 3D acinar structures requires glucocorticoid and JNK signaling.

Mammary epithelial cells cultured on a concentrated laminin-rich extracellular matrix formed 3D acinar structures that matured to polarized monolayers surrounding a lumen. In the absence of glucocorticoids mature acinus formation failed and the expression of an acinus-associated, activator protein 1 (AP1) and nuclear factor kappaB transcription factor DNA-binding profile was lost. Treatment with the JNK inhibitor, SP600125, caused similar effects, whereas normal organization of the mammary epithelial cells as acini caused JNK activation in a glucocorticoid-dependent manner. The forming acini expressed BRCA1, GADD45beta, MEKK4, and the JNK activating complex GADD 45beta-MEKK4 in a glucocorticoid-dependent fashion. JNK catalyzed phosphorylation of c-Jun was also detected in the acini. In addition, expression of beta4 integrin and in situ occupation of its promoter by AP1 components, c-Jun and Fos, was glucocorticoid dependent. These results suggest that glucocortocoid signaling regulates acinar integrity through a pathway involving JNK regulation of AP1 transcription factors and beta4 integrin expression.[1]


  1. Organization of mammary epithelial cells into 3D acinar structures requires glucocorticoid and JNK signaling. Murtagh, J., McArdle, E., Gilligan, E., Thornton, L., Furlong, F., Martin, F. J. Cell Biol. (2004) [Pubmed]
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