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. 2018 Aug 6;8:299. doi: 10.3389/fonc.2018.00299

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Copyright © 2018 Rappaport and Waldman.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Suppression of cGMP signaling promotes epithelial transformation. Basal cGMP tone in the intestinal epithelium promotes epithelial homeostasis. cGMP, through its effector, PKG, regulates several downstream mechanisms including mucus hydration, metabolism, inflammation, barrier integrity, DNA damage sensing, and cell cycle progression. In contrast, intestinal transformation is characterized by upregulation of phosphodiesterases and suppression of GUCY2C paracrine ligands, reducing intracellular cGMP and producing an epithelial phenotype predisposed to cancer progression. cGMP, cyclic guanosine monophosphate; GTP, guanosine triphosphate; GUCY2C, guanylate cyclase C; HGF, hepatocyte growth factor; IFNγ interferon gamma; PDE, phosphodiesterase; PKG, protein kinase G; TGFβ, transforming growth factor beta; TNFα tumor necrosis factor alpha; 5′-AMP, 5′-adenosine monophosphate; 5′-GMP, 5′-guanosine monophosphate.