Interferon-y-Induced Growth Inhibition of Neuroblastoma Cells is Independent of Induction of Nitric Oxide Synthase and Indoleamine 2,3-dioxygenase
Leitner Stephan,
Golderer Georg,
Winkler Christiana,
Fuchs Dietmar,
Werner-Felmayer Gabriele,
Werner Ernst R.
Affiliations
Leitner Stephan
Institute for Medical Chemistry and Biochemistry, Medical University of Innsbruck, Fritz-Pregl-Str.3, A-6020 Innsbruck, Austria
Golderer Georg
Institute for Medical Chemistry and Biochemistry, Medical University of Innsbruck, Fritz-Pregl-Str.3, A-6020 Innsbruck, Austria
Winkler Christiana
Institute for Medical Chemistry and Biochemistry, Medical University of Innsbruck, Fritz-Pregl-Str.3, A-6020 Innsbruck, Austria
Fuchs Dietmar
Institute for Medical Chemistry and Biochemistry, Medical University of Innsbruck, Fritz-Pregl-Str.3, A-6020 Innsbruck, Austria
Werner-Felmayer Gabriele
Institute for Medical Chemistry and Biochemistry, Medical University of Innsbruck, Fritz-Pregl-Str.3, A-6020 Innsbruck, Austria
Werner Ernst R.
Institute for Medical Chemistry and Biochemistry, Medical University of Innsbruck, Fritz-Pregl-Str.3, A-6020 Innsbruck, Austria, Phone: ++43 512 507 3519, Fax: ++43 5 Ρ 507 2865
We investigated a possible involvement of nitric oxide formed by inducible nitric oxide synthase (iNOS) in the signaling cascade leading to growth inhibition and differentiation in the human neuroblastoma cell line SK-NSII. Treatment of SK-N-SH with interferon-γ (IFN-γ) plus interleukin-lß (IL-lß) led to induction of iNOS, growth inhibition and an altered cell shape. However two inhibitors of iNOS were not able to prevent cytokine induced changes. In addition, IFN-γ alone led to growth inhibition in absence of iNOS induction. Inhibition of the induced indoleamine 2,3-dioxygenase (IDO) activity also did not prevent growth inhibition. Our findings show that mechanisms other than NO and IDO can control interferon-y-induced growth inhibition of SK-N-SH cells.