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Overexpression of proline oxidase induces proline-dependent and mitochondria-mediated apoptosis

  1. Author:
    Hu, C. A. A.
    Donald, S. P.
    Yu, J.
    Lin, W. W.
    Liu, Z. H.
    Steel, G.
    Obie, C.
    Valle, D.
    Phang, J. M.

  2. Author Address

    Univ New Mexico, Sch Med, Dept Biochem & Mol Biol, Albuquerque, NM 87131 USA. Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA. Tri Serv Gen Hosp, Dept Psychiat, Taipei, Taiwan. Natl Def Med Inst, Taipei, Taiwan. Johns Hopkins Univ, Howard Hughes Med Inst, McKusick Nathans Inst Genet Med, Sch Med, Baltimore, MD 21218 USA.;Valle, D, NCI, Metab & Canc Susceptibil Sect, Basic Res Lab, 1050 Boyles St,Bldg 538,Room 115, Frederick, MD 20895 USA.;dvalle@jhmi.edu phang@ncifcrf.gov
    1. Year: 2007
    2. Date: Jan
  2. Journal: Molecular and Cellular Biochemistry
    1. 295
    2. 1-2
    3. Pages: 85-92
  4. Type of Article: Article
  5. ISSN: 0300-8177
  1. Abstract:

    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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External Sources

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  2. DOI: 10.1007/s11010-006-9276-6
  3. View record in Web of Science®
  4. WOS: 000243659600011

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