RKIP does not contribute to MAP kinase pathway silencing in the Merkel Cell Carcinoma cell line UISO

Roland Houben^* , Sonja Ortmann^* and Juergen C Becker

Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie, Julius-Maximilians-Universität, Josef-Schneider-Str. 2, D-97080 Würzburg, Germany

author email corresponding author email* Contributed equally

Journal of Carcinogenesis 2007, 6:16doi:10.1186/1477-3163-6-16


Published:	24 October 2007

Abstract

Background

The Raf kinase inhibitor protein (RKIP) has been shown to block MAP kinase pathway as well as NFκB signalling. By means of immunohistochemistry, we previously demonstrated that the MAP kinase pathway is virtually inactive in Merkel cell carcinoma (MCC). Similarly to MCC in situ high RKIP expression accompanies absence of ERK phosphorylation in the MCC cell line UISO suggesting that RKIP might be causative for MAP kinase pathway silencing.

Methods

Applying an siRNA approach RKIP expression was knocked down in UISO cells and a possible influence on MAP kinase pathway activity was assessed by Western blot analysis using phospho-specific antibodies. Moreover, a possible effect of RKIP knock down in UISO cells on proliferation as well as chemosensitivity to cisplatin were examined applying the MTS assay.

Results

Surprisingly the absence of phosphorylation of the MAP kinases ERK1 and ERK 2 even following growth factor stimulation was not affected by the RKIP knock down indicating that RKIP is not essential for blocking the MAP kinase pathway in the MCC cell line UISO. Moreover, proliferation as well as chemosensitivity towards cisplatin were not altered upon knock down of RKIP.