1. ¹German Cancer Research Center, Molecular Therapy of Virus-Associated Cancers (F065), Im Neuenheimer Feld 242, 69120 Heidelberg, Germany
2. ²Department of Urology, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany
3. ³Department of Pathology, University of Heidelberg, Im Neuenheimer Feld 220/221, 69120 Heidelberg, Germany
4. ⁴German Cancer Research Center, Cellular and Molecular Pathology (E090), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany
5. ⁵German Cancer Research Center, Electron Microscopy (F090), Im Neuenheimer Feld 242, 69120 Heidelberg, Germany
6. ⁶Department of Medical Biometry, University of Heidelberg, Im Neuenheimer Feld 305, 69120 Heidelberg, Germany

Correspondence: Professor F Hoppe-Seyler, E-mail: hoppe-seyler@dkfz.de

Received 21 May 2007; Revised 5 September 2007; Accepted 5 September 2007.

Abstract

The antiapoptotic Livin/ML-IAP gene has recently gained much attention as a potential new target for cancer therapy. Reports indicating that livin is expressed almost exclusively in tumours, but not in the corresponding normal tissue, suggested that the targeted inhibition of livin may present a novel tumour-specific therapeutic strategy. Here, we compared the expression of livin in renal cell carcinoma and in non-tumorous adult kidney tissue by quantitative real-time reverse transcription-PCR, immunoblotting, and immunohistochemistry. We found that livin expression was significantly increased in tumours (P=0.0077), but was also clearly detectable in non-tumorous adult kidney. Transcripts encoding Livin isoforms and were found in both renal cell carcinoma and normal tissue, without obvious qualitative differences. Livin protein in renal cell carcinoma samples exhibited cytoplasmic and/or nuclear staining. In non-tumorous kidney tissue, Livin protein expression was only detectable in specific cell types and restricted to the cytoplasm. Thus, whereas the relative overexpression of livin in renal cell carcinoma indicates that it may still represent a therapeutic target to increase the apoptotic sensitivity of kidney cancer cells, this strategy is likely to be not tumour-specific.