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Expression of Integrin-linked Kinase Is Increased in Differentiated Cells

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

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

Correspondence to: Nils Cordes, OncoRay–Center for Radiation Research in Oncology, Medical Faculty Carl Gustav Carus, Dresden University of Technology, Fetscherstrasse 74/PF 86, 01307 Dresden, Germany. E-mail: nils.cordes{at}oncoray.de

Integrin-linked kinase (ILK), a mediator of β integrin signals, has emerged as a therapeutic target in malignant tumors. Because 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 tissues, 181 normal tissues), immunohistochemistry was performed [ILK, Akt, phospho-Akt-S473, loricrin, transforming growth factor β2 (TGFβ2)], and staining intensities were semiquantitatively 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 colocalized with its putative downstream target Akt and with loricrin or TGFβ2. Our findings clearly show 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. (J Histochem Cytochem 56:819–829, 2008)

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

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