Expression of Integrin-linked Kinase Is Increased in Differentiated Cells

Michael Haase ¹, Christine C. Gmach ¹, Iris Eke ¹, Stephanie Hehlgans ¹, Gustavo B. Baretton ¹ and Nils Cordes ^1*

¹ OncoRay – Center for Radiation Research in Oncology (MH,CCG,IE,SH,NC) and Department of Pathology (GBB), Medical Faculty Carl Gustav Carus, Dresden University of Technology, Dresden, Germany

^* To whom correspondence should be addressed. E-mail: nils.cordes{at}oncoray.de.

Submitted on February 11, 2008
Accepted on 13 May 2008

	Abstract

Integrin-linked kinase (ILK), a mediator of integrin signals, has emerged as a therapeutic target in malignant tumors. As malignant transformation is accompanied by dedifferentiation, ILK expression was evaluated in diverse normal and tumor tissue samples with regard to tissue differentiation. In single sections and in a tissue microarray (323 tumor, 181 normal tissues), immunohistochemistry was performed [ILK, Akt, phospho-Akt-S473, loricrin, transforming growth factor 2 (TGF2)] and staining intensities were semi-quantitatively scored. Increased ILK expression was clearly associated with increased differentiation in normal gastrointestinal, neural, bone marrow, renal tissue and in more differentiated areas of malignant tumors. ILK co-localized with its putative downstream target Akt and with loricrin or TGF2. Our findings clearly demonstrate that elevated levels of ILK are associated with cellular differentiation in high turnover tissues but not generally with a malignant phenotype. Our study indicates that ILK is not a general molecular target for cancer therapy but rather an indicator of differentiation. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

Key Words: integrin-linked kinase, differentiation, tumor, normal tissue, tissue microarray

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