Wnt, hedgehog, and snail: sister pathways that control by GSK-3beta and beta-Trcp in the regulation of metastasis

BP Zhou, MC Hung - Cell Cycle, 2005 - Taylor & Francis
Cell Cycle, 2005Taylor & Francis
The epithelial-mesenchymal transition have begun to attracted many attentions as a
potentialmechanism for metastasis. The phenotypic changes of increased motility and
invasiveness of cancercells are reminiscent of epithelial-mesenchymal transition (EMT) that
associates with thedownregulation of E-cadherin. Snail, zinc finger transcription factor,
triggers this process by repressingE-cadherin expression. Recently Snail was found to be
dually regulated GSK-3beta through proteinstability and cellular localization. The …
The epithelial-mesenchymal transition have begun to attracted many attentions as a potentialmechanism for metastasis. The phenotypic changes of increased motility and invasiveness of cancercells are reminiscent of epithelial-mesenchymal transition (EMT) that associates with thedownregulation of E-cadherin. Snail, zinc finger transcription factor, triggers this process by repressingE-cadherin expression. Recently Snail was found to be dually regulated GSK-3beta through proteinstability and cellular localization. The involvement of GSK-3beta and beta-Trcp in the regulation of Snail isparticular interesting, because these two molecules are also known to involve in the regulation of Wntand hedgehog pathways that are known to control cell fate and morphogenesis during development andtumorigenesis. Here, we briefly compare these pathways and propose the possibility of crosss-talkamong these pathways in the regulation of cell adhesion, cell fate, and migration during metastasis.
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