Accessible Requires Authentication Published by De Gruyter November 13, 2012

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

Steffen Kraus, Maximilian Fruth, Thea Bunsen and Dorit K. Nägler
From the journal Biological Chemistry

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.


Corresponding author: Dorit K. Nägler, Experimental Surgery and Regenerative Medicine, Department of Surgery, Ludwig-Maximilians-University, D-80336 Munich, Germany

Received: 2012-5-18
Accepted: 2012-9-19
Published Online: 2012-11-13
Published in Print: 2012-12-01

©2012 by Walter de Gruyter Berlin Boston