E-cadherin and, in its absence, N-cadherin promotes nanog expression in mouse embryonic stem cells via STAT3 Phosphorylation

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Abstract

We have recently shown that loss of E-cadherin in mouse embryonic stem cells (mESCs) results in significant alterations to both the transcriptome and hierarchy of pluripotency-associated signaling pathways. Here, we show that E-cadherin promotes kruppel-like factor 4 (Klf4) and Nanog transcript and protein expression in mESCs via STAT3 phosphorylation and that β-catenin, and its binding region in E-cadherin, is required for this function. To further investigate the role of E-cadherin in leukemia inhibitory factor (LIF)-dependent pluripotency, E-cadherin null (Ecad-/-) mESCs were cultured in LIF/bone morphogenetic protein supplemented medium. Under these conditions, Ecad-/- mESCs exhibited partial restoration of cell-cell contact and STAT3 phosphorylation and upregulated Klf4, Nanog, and N-cadherin transcripts and protein. Abrogation of N-cadherin using an inhibitory peptide caused loss of phospho STAT3, Klf4, and Nanog in these cells, demonstrating that N-cadherin supports LIF-dependent pluripotency in this context. We therefore identify a novel molecular mechanism linking E- and N-cadherin to the core circuitry of pluripotency in mESCs. This mechanism may explain the recently documented role of E-cadherin in efficient induced pluripotent stem cell reprogramming. © AlphaMed Press.

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Hawkins, K., Mohamet, L., Ritson, S., Merry, C. L. R., & Ward, C. M. (2012). E-cadherin and, in its absence, N-cadherin promotes nanog expression in mouse embryonic stem cells via STAT3 Phosphorylation. Stem Cells, 30(9), 1842–1851. https://doi.org/10.1002/stem.1148

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