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IGF-I receptor phosphorylation is impaired in cathepsin X-deficient prostate cancer cells.
MedLine Citation:
PMID:  23152410     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Abstract The cysteine-type peptidase cathepsin X is highly upregulated in several cancers and presumably promotes tumor invasion through bypassing cellular senescence. Here, we present first evidence that the underlying mechanism may involve the regulation of the insulin-like growth factor (IGF) system, a well-known activator of proliferating tumor cells. Cathepsin X deficiency leads to a reduced phosphorylation of the IGF-I receptor in response to IGF-I stimulation. In addition, downstream signaling through focal adhesion kinase was also affected. Taken together, our results indicate that cathepsin X is able to assist in IGF signaling, which may be an important progress toward understanding cathepsin X-dependent tumorigenesis.
Authors:
Steffen Kraus; Maximilian Fruth; Thea Bunsen; Dorit K Nägler
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Biological chemistry     Volume:  393     ISSN:  1437-4315     ISO Abbreviation:  Biol. Chem.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-15     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9700112     Medline TA:  Biol Chem     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1457-62     Citation Subset:  IM    
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