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The insulin-like growth factor I receptor protects tumor cells from apoptosis in vivo
M Resnicoff1, D Abraham, W Yutanawiboonchai
1Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Abstract:
The role of the insulin-like growth factor I receptor (IGF-IR) in programmed cell death has been investigated in vivo in a biodiffusion chamber, where the extent of cell death could be determined quantitatively. We found that a decrease in the number of IGF-IRs causes massive apoptosis in vivo in several transplantable tumors, either from humans or rodents. Conversely, an overexpressed IGF-IR protects cells from apoptosis in vivo. We also show that the same conditions that in vitro cause only partial growth arrest with a minimum of cell death, induce in vivo almost complete cell death. We conclude that the IGF-IR activated by its ligands plays a very important protective role in programmed cell death, and that its protective action is even more striking in vivo than in vitro.
Insights
The insulin-like growth factor I receptor (IGF-IR) protects cells from programmed cell death. Its protective role is more significant in vivo than in vitro, especially in tumors.
Area of Science:
- Cell Biology
- Cancer Research
- Molecular Biology
Background:
- Programmed cell death, or apoptosis, is crucial for tissue homeostasis.
- The insulin-like growth factor I receptor (IGF-IR) is implicated in cell growth and survival.
- Understanding IGF-IR's role in apoptosis is vital for cancer therapy development.
Purpose of the Study:
- To investigate the role of IGF-IR in programmed cell death in vivo.
- To quantify the effect of IGF-IR levels on apoptosis in transplantable tumors.
- To compare the impact of IGF-IR on cell death in vitro versus in vivo.
Main Methods:
- Utilized a biodiffusion chamber for in vivo cell death determination.
- Examined apoptosis in transplantable human and rodent tumors.
- Manipulated IGF-IR expression levels (downregulation and overexpression).
Main Results:
- Decreased IGF-IR levels led to massive apoptosis in vivo across various tumors.
- Overexpressed IGF-IR conferred protection against apoptosis in vivo.
- Conditions causing minimal cell death in vitro induced near-complete cell death in vivo.
Conclusions:
- IGF-IR activation by ligands plays a critical protective role in programmed cell death.
- The protective effect of IGF-IR against apoptosis is more pronounced in vivo than in vitro.
- IGF-IR modulation presents a potential therapeutic target for enhancing cancer cell death.