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.
| Item Type: | Journal article |
|---|---|
| Form of publication: | Publisher's Version |
| Faculties: | Medicine |
| Subjects: | 500 Science > 540 Chemistry |
| URN: | urn:nbn:de:bvb:19-epub-17692-7 |
| ISSN: | 1431-6730 |
| Alliance/National Licence: | This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively. |
| Language: | English |
| Item ID: | 17692 |
| Date Deposited: | 02. Jan 2014 10:28 |
| Last Modified: | 04. Nov 2020 12:59 |

