Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 295, Issue 1-2, Pages 85-92Publisher
SPRINGER
DOI: 10.1007/s11010-006-9276-6
Keywords
proline oxidase; apoptosis; reactive oxygen species; mitochondria; p53; proline-P5C cycle
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Funding
- Intramural NIH HHS Funding Source: Medline
- NCI NIH HHS [R01 CA106644, 1 R01 CA106644-01] Funding Source: Medline
- NCRR NIH HHS [P20 RR016480] Funding Source: Medline
- DIVISION OF BASIC SCIENCES - NCI [Z01BC000157] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [Z01BC010743, R01CA106644] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016480] Funding Source: NIH RePORTER
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Proline oxidase (POX), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of proline to pyrroline-5-carboxylate (P5C). Previously we showed that overexpression of POX is associated with generation of reactive oxygen species (ROS) and apoptosis in POX-inducible colorectal cancer cells, DLD-1.POX. We also showed expression of mitochondrial MnSOD partially blunts POX-induced ROS generation and apoptosis. To further investigate the molecular basis of POX-induced apoptosis, we utilized the DLD-1.POX cells to show that cells overproducing POX exhibit an L-proline-dependent apoptotic response. The apoptotic effect is specific for L-proline, detectable at 0.2 mM, maximal at 1 mM, and occurs during 48-72 h following the addition of L-proline to cells with maximally induced POX. The apoptotic response is mitochondria-mediated with release of cytochrome c, activation of caspase-9, chromatin condensation/DNA fragmentation, and cell shrinkage. We conclude that in the presence of proline, high POX activity is sufficient to induce mitochondria-mediated apoptosis.
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