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

Rac-dependent cyclin D1 gene expression regulated by cadherin- and integrin-mediated adhesion.

Integrin-mediated adhesion to substratum is required for cyclin D1 induction in mesenchymal cells, but we show here that the induction of cyclin D1 persists despite blockade of ECM-integrin signaling in MCF10A mammary epithelial cells. E-cadherin-mediated cell-cell adhesion also supports cyclin D1 induction in these cells, and the combined inhibition of both E-cadherin and integrin adhesion is required to prevent the expression of cyclin D1 mRNA and protein. Our previous studies described a pro-proliferative effect of E-cadherin in MCF10A cells, mediated by Rac, and we now show that Rac is required for cyclin D1 mRNA induction by both E-cadherin and integrin engagement. The levels of p21Cip1 and p27Kip1, Cdk inhibitors that are also targets of integrin signaling, are not affected by E-cadherin-mediated cell-cell adhesion. Finally, we show that the increased expression of cyclin D1 mRNA associated with E-cadherin-dependent cell-cell adhesion is causally linked to an increased entry into S phase. Our results identify Rac signaling to cyclin D1 as a crucial pro-proliferative effect of E-cadherin-mediated cell-cell adhesion.[1]


  1. Rac-dependent cyclin D1 gene expression regulated by cadherin- and integrin-mediated adhesion. Fournier, A.K., Campbell, L.E., Castagnino, P., Liu, W.F., Chung, B.M., Weaver, V.M., Chen, C.S., Assoian, R.K. J. Cell. Sci. (2008) [Pubmed]
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