Oncogenic c-H-ras deregulates survivin expression: an improvement for survival |
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Authors: | Sommer Klaus W Rodgarkia-Dara Chantal J Schreiner Claudia Holzmann Klaus Krupitza Georg Cerni Christa |
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Affiliation: | Clinics of Internal Medicine I, Division Institute of Cancer Research, Medical University of Vienna, Borschkegasse 8a, 1090 Vienna, Austria. |
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Abstract: | Survivin protein accomplishes two basic functions: cell cycle regulation and control of apoptosis. It is only expressed in G2/M phase and it influences rescue pathways in apoptosis-induced cells. Overexpression of constitutive active c-H-ras in HeLa, or induction of c-H-ras in a stable HeLaDiR cell line, led to sustained survivin expression in all cell cycle phases and even protected cells from drug induced apoptosis. siRNA-mediated silencing of survivin reversed this protection. Here we link the anti-apoptotic property of survivin to its cell cycle (in)dependent regulation via the activity of oncogenic c-H-ras. |
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Keywords: | IAP, inhibitor of apoptosis protein DiR, dexamethasone inducible ras Dex, dexamethasone |
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