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.
journal_name
Biol Chemjournal_title
Biological chemistryauthors
Kraus S,Fruth M,Bunsen T,Nägler DKdoi
10.1515/hsz-2012-0209subject
Has Abstractpub_date
2012-12-01 00:00:00pages
1457-62issue
12eissn
1431-6730issn
1437-4315pii
/j/bchm.2012.393.issue-12/hsz-2012-0209/hsz-2012-0journal_volume
393pub_type
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