Skip NavigationSkip to Content
Return Return to Search Results

Proline metabolism and cancer

  1. Author:
    Phang, J. M.
    Liu, W.

  2. Author Address

    [Phang, James M.; Liu, Wei] NCI Frederick, Metab & Canc Susceptibil Sect, Comparat Carcinogenesis Lab, Ctr Canc Res, Frederick, MD 21702 USA.;Phang, JM (reprint author), NCI Frederick, Metab & Canc Susceptibil Sect, Comparat Carcinogenesis Lab, Ctr Canc Res, Frederick, MD 21702 USA;phangj@mail.nih.gov
    1. Year: 2012
    2. Date: Jan
  2. Journal: Frontiers in Bioscience-Landmark
    1. 17
    2. Pages: 1835-1845
  4. Type of Article: Article
  5. ISSN: 1093-9946
  1. Abstract:

    Proline plays a special role in cancer metabolism. Proline oxidase (POX), a.k.a. proline dehydrogenase (PRODH), is among a few genes induced rapidly and robustly by P53, the tumor suppressor. Ectopic expression of POX under control of tet-off promoter initiated mitochondrial apoptosis. The mechanism activated by POX is mediated by its production of ROS. In immunodeficient mice, POX overexpression markedly retarded growth of xenograft tumors. In human tumors of the digestive tract and kidney, POX was markedly decreased, suggesting that the suppressive effect of POX was downregulated. This was not due to POX gene mutations or hypermethylation. Instead, a microRNA, miR-23b*, expressed at high levels in tumors, was a potent inhibitor of POX expression. Furthermore, antagomirs of miR-23b* reversed the downregulated expression of POX and its tumor-suppressive effect, thereby providing a therapeutic strategy. POX not only responds to genotoxic stress, but also to inflammatory and metabolic stress. Depending on microenvironmental and temporal factors, POX can mediate oppositely-directed responses-programmed cell death, on the one hand, and survival, on the other.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.2741/4022
  3. View record in Web of Science®
  4. WOS: 000300054400017

Library Notes

  1. Fiscal Year: FY2011-2012
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel