Document Detail

Critical role of Wnt5a-Ror2 signaling in motility and invasiveness of carcinoma cells following Snail-mediated epithelial-mesenchymal transition.
MedLine Citation:
PMID:  21342370     Owner:  NLM     Status:  In-Data-Review    
Expression of Snail has been shown to mediate epithelial-mesenchymal transition (EMT) of epithelial cells and carcinomas, characterized by morphological alterations with disappearance and appearance of E-cadherin and vimentin, respectively. Here, we show that ectopic expression of Snail in human epidermoid carcinoma A431 cells (Snail/A431) induces the representative EMT, resulting in remarkable motile and invasive properties of the cells. Expression of Wnt5a, its receptor Ror2 and matrix metalloproteinase (MMP)-2 is induced in Snail/A431, but not in control A431 cells. Interestingly, suppressed expression of either Wnt5a or Ror2 in Snail/A431 cells results in the inhibition of in vitro cell motility and invasiveness, at least partly mediated by MMP-2, without affecting characteristics of EMT, i.e., mesenchymal morphology, and down- and up-regulations of E-cadherin and vimentin, respectively. We further show that endogenous Snail is required for sustained expression of Wnt5a, Ror2 and MMP-13 in human osteosarcoma SaOS-2 cells. The results indicate that expression of both Wnt5a and Ror2 is induced during Snail-mediated EMT or malignant progression of cancer cells and that consequently activated Wnt5a-Ror2 signaling confers highly motile and invasive properties on cancer cells. Thus, Wnt5a-Ror2 signaling can be a target of cancer therapies to prevent cancer cells from undergoing invasion and metastasis.
Dayong Ren; Yasuhiro Minami; Michiru Nishita
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Genes to cells : devoted to molecular & cellular mechanisms     Volume:  16     ISSN:  1365-2443     ISO Abbreviation:  Genes Cells     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9607379     Medline TA:  Genes Cells     Country:  England    
Other Details:
Languages:  eng     Pagination:  304-15     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. Journal compilation © 2011 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd.
Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
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