Journal
CELL DEATH AND DIFFERENTIATION
Volume 7, Issue 7, Pages 654-665Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4400693
Keywords
caspase; mitochondria; mannitol; SHEP; IGF-IR
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Funding
- NCI NIH HHS [R01CA69276, 3T32CA09676] Funding Source: Medline
- NINDS NIH HHS [R01NS36778] Funding Source: Medline
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The type I insulin-like growth factor receptor (IGF-IR) is important for mitogenesis, transformation, and survival of tumor cells. The current study examines the effect of IGF-IR expression and activation on apoptosis in SHEP human neuroblastoma cells. SHEP cells undergo apoptosis which is prevented by IGF-I addition or overexpression of the IGF-IR (SHEP/IGF-IR cells). High mannitol treatment activates caspase-3 by 1 h in SHEP cells while caspase-3 activation is delayed by 3 h in SHEP/IGF-IR cells. Transfection with Bcl-2 (SHEP/Bcl-2 cells) prevents serum withdrawal and mannitol induced apoptosis and caspase-3 activation. Mannitol induces mitochondrial membrane depolarization in both SHEP and SHEP/IGF-IR cells. IGF-IR activation or overexpression of Bcl-2 in SHEP cells prevents mitochondrial membrane depolarization. Collectively, these results suggest that IGF-IR or Bcl-2 overexpression in neuroblastoma cells promotes cell survival by preventing mitochondrial membrane depolarization and caspase-3 activation, ultimately leading to increased tumor growth.
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