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. Author manuscript; available in PMC: 2014 Oct 24.
Published in final edited form as: Transl Androl Urol. 2013 Sep 1;2(3):202–211. doi: 10.3978/j.issn.2223-4683.2013.09.04

Figure 1.

Figure 1

EMT control by the AR signaling. EMT in prostate epithelial cells is mediated by TGF-β and AR signaling interactions. AR induces EMT through activation of Snail transcription factor or via repression of E-cadherin. Activation of Snail, ZEB-1 or Smad transcription factors initiates allows for mesenchymal gene expression. Snail increases the expression of mesenchymal markers and proteins associated with invasion. E-cadherin is transciptionally suppressed by Snail; this loss of E-cadherin, which mediates intracellular adhesions at adherens junctions, leads to collapse of cell-cell communications and onset of EMT. Cripto-1 is a critical effector of the TGF-(3 signaling that upregulates mesenchymal expression during embryonic development. ZEB-1 is involved in a feedback loop with AR where downregulation of AR leads to uncontrolled ZEB-1 expression