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

Roland Houben1, Sonja Ortmann1, Juergen C Becker1

  • 1Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie, Julius-Maximilians-Universität, Josef-Schneider-Str. 2, D-97080 Würzburg, Germany.

Journal of Carcinogenesis
|October 26, 2007
PubMed
Abstract

Insights

Raf kinase inhibitor protein (RKIP) does not silence the MAP kinase pathway in Merkel cell carcinoma (MCC). RKIP knockdown in MCC cells did not affect MAP kinase activity, proliferation, or cisplatin sensitivity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Raf kinase inhibitor protein (RKIP) inhibits MAP kinase and NFkappaB signaling.
  • Merkel cell carcinoma (MCC) exhibits an inactive MAP kinase pathway.
  • High RKIP expression correlates with absent ERK phosphorylation in MCC cells.

Purpose of the Study:

  • To investigate the role of RKIP in silencing the MAP kinase pathway in MCC.
  • To determine if RKIP knockdown affects proliferation and chemosensitivity in MCC cells.

Main Methods:

  • Small interfering RNA (siRNA) was used to knock down RKIP expression in the UISO MCC cell line.
  • Western blot analysis with phospho-specific antibodies assessed MAP kinase pathway activity.
  • MTS assay evaluated proliferation and cisplatin chemosensitivity.

Main Results:

  • RKIP knockdown did not restore MAP kinase pathway activity (ERK1/2 phosphorylation) in UISO cells, even after growth factor stimulation.
  • Proliferation of UISO cells was not altered by RKIP knockdown.
  • RKIP knockdown did not affect the chemosensitivity of UISO cells to cisplatin.

Conclusions:

  • RKIP is not essential for silencing the MAP kinase pathway in the UISO MCC cell line.
  • RKIP does not play a significant role in regulating proliferation or cisplatin sensitivity in this MCC model.

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