IGF-I receptor phosphorylation is impaired in cathepsin X-deficient prostate cancer cells.

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 Chem

journal_title

Biological chemistry

authors

Kraus S,Fruth M,Bunsen T,Nägler DK

doi

10.1515/hsz-2012-0209

subject

Has Abstract

pub_date

2012-12-01 00:00:00

pages

1457-62

issue

12

eissn

1431-6730

issn

1437-4315

pii

/j/bchm.2012.393.issue-12/hsz-2012-0209/hsz-2012-0

journal_volume

393

pub_type

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