| IGF-I receptor phosphorylation is impaired in cathepsin X-deficient prostate cancer cells. | |
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MedLine Citation:
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PMID: 23152410 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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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. |
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Authors:
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Steffen Kraus; Maximilian Fruth; Thea Bunsen; Dorit K Nägler |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Biological chemistry Volume: 393 ISSN: 1437-4315 ISO Abbreviation: Biol. Chem. Publication Date: 2012 Dec |
Date Detail:
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Created Date: 2012-11-15 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9700112 Medline TA: Biol Chem Country: Germany |
Other Details:
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Languages: eng Pagination: 1457-62 Citation Subset: IM |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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