Oncogenic c-H-ras deregulates survivin expression: an improvement for survival.
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.
Sommer
Klaus W
KW
Clinics of Internal Medicine I, Division Institute of Cancer Research, Medical University of Vienna, Borschkegasse 8a, 1090 Vienna, Austria.
Rodgarkia-Dara
Chantal J
CJ
Schreiner
Claudia
C
Holzmann
Klaus
K
Krupitza
Georg
G
Cerni
Christa
C
D017209:Apoptosis; D002453:Cell Cycle; D004317:Doxorubicin / Q000037:antagonists & inhibitors / Q000633:toxicity; D006367:HeLa Cells; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015689:Oncogene Protein p21(ras) / Q000378:metabolism*; D034622:RNA Interference; D000077022:Survivin
C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins; D009363:Neoplasm Proteins; D000077022:Survivin; D004317:Doxorubicin; D015689:Oncogene Protein p21(ras)