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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cathepsin Z / genetics*
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Cathepsin Z / metabolism
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Cathepsins / genetics*
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Cathepsins / metabolism
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Cell Line, Tumor
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Cellular Senescence
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Focal Adhesion Protein-Tyrosine Kinases / metabolism
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Humans
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Male
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Phosphorylation
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Prostate / cytology
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Prostate / metabolism*
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Prostate / pathology
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Prostatic Neoplasms / genetics*
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Prostatic Neoplasms / metabolism*
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Prostatic Neoplasms / pathology
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Protein Precursors / genetics*
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Protein Precursors / metabolism
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RNA Interference
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Receptor, IGF Type 1 / metabolism*
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Signal Transduction
Substances
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Protein Precursors
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Receptor, IGF Type 1
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Focal Adhesion Protein-Tyrosine Kinases
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Cathepsins
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procathepsin X, human
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CTSZ protein, human
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Cathepsin Z