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Lack of oxidative phosphorylation and low mitochondrial membrane potential decrease susceptibility to apoptosis and
1Department of Neurology, University of Miami, School of Medicine, Miami, Florida 33136, USA.
The Journal of Biological Chemistry
|March 4, 2000
Summary
Cells lacking mitochondrial oxidative phosphorylation showed resistance to apoptosis, suggesting a role in cancer development. Bcl-x(L) protein may offer protection by inhibiting caspase activation.
Area of Science:
- Cell Biology
- Biochemistry
- Cancer Research
Background:
- Mitochondrial membrane potential (DeltaPsim) and oxidative phosphorylation are crucial for apoptosis.
- The role of these factors in cancer cell survival remains incompletely understood.
Purpose of the Study:
- To investigate the impact of impaired mitochondrial function on apoptosis in osteosarcoma cells.
- To explore the role of Bcl-x(L) in modulating apoptosis and mitochondrial function.
Main Methods:
- Osteosarcoma cell lines with and without mitochondrial DNA were used.
- Cells were exposed to staurosporine to induce apoptosis.
- Mitochondrial membrane potential, oxidative phosphorylation, caspase activation, and cytochrome c release were assessed.
Main Results:
- Cells lacking mitochondrial DNA exhibited low DeltaPsim and impaired oxidative phosphorylation, yet showed increased resistance to staurosporine-induced death.
- This resistance correlated with decreased caspase 3 activation, but not with mitochondrial permeability transition pore opening or cytochrome c release.
- Bcl-x(L) conferred protection against apoptosis and caspase 3 activation, independent of mitochondrial function, but could stimulate respiration in cells with mitochondrial DNA.
Conclusions:
- Lack of functional oxidative phosphorylation and/or low DeltaPsim is associated with an antiapoptotic effect, potentially contributing to cancer development.
- Bcl-x(L) may exert antiapoptotic effects by stimulating oxidative phosphorylation and/or inhibiting caspase activation.
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