Logo Logo
Hilfe
Hilfe
Switch Language to English

Kraus, Steffen; Fruth, Maximilian; Bunsen, Thea und Nägler, Dorit K. (2012): IGF-I receptor phosphorylation is impaired in cathepsin X-deficient prostate cancer cells. In: Biological Chemistry, Bd. 393, Nr. 12: S. 1457-1462 [PDF, 691kB]

[thumbnail of hsz-2012-0209.pdf]
Vorschau
Download (691kB)

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.

Dokument bearbeiten Dokument bearbeiten