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    P53 suppresses expression of the 14-3-3gamma oncogene

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    Author
    Radhakrishnan, Vijayababu
    Putnam, Charles
    Qi, Wenqing
    Martinez, Jesse
    Affiliation
    Arizona Cancer Center, Department of Cellular & Molecular Medicine, University of Arizona, Tucson, Arizona 85724, USA
    Department of Pediatrics, Steele Research Center, 1501 N Campbell Ave, Tucson, Arizona 85724, USA
    Department of Surgery, 1501 N Campbell ave, Tucson, Arizona 85724, USA
    Department of Medicine, 1515 N. Campbell Ave., Tucson, Arizona 85724, USA
    Issue Date
    2011
    Keywords
    Lung cancer
    14-3-3
    p53 mutations
    Gene Copy
    Transcription Regulation
    
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    Publisher
    BioMed Central
    Citation
    Radhakrishnan et al. BMC Cancer 2011, 11:378 http://www.biomedcentral.com/1471-2407/11/378
    Journal
    BMC Cancer
    Rights
    © 2011 Radhakrishnan et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
    Collection Information
    This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
    Abstract
    BACKGROUND:14-3-3 proteins are a family of highly conserved proteins that are involved in a wide range of cellular processes. Recent evidence indicates that some of these proteins have oncogenic activity and that they may promote tumorigenesis. We previously showed that one of the 14-3-3 family members, 14-3-3gamma, is over expressed in human lung cancers and that it can induce transformation of rodent cells in vitro.METHODS:qRTPCR and Western blot analysis were performed to examine 14-3-3gamma expression in non-small cell lung cancers (NSCLC). Gene copy number was analyzed by qPCR. P53 mutations were detected by direct sequencing and also by western blot. CHIP and yeast one hybrid assays were used to detect p53 binding to 14-3-3gamma promoter.RESULTS:Quantitative rtPCR results showed that the expression level of 14-3-3gamma was elevated in the majority of NSCLC that we examined which was also consistent with protein expression. Further analysis of the expression pattern of 14-3-3gamma in lung tumors showed a correlation with p53 mutations suggesting that p53 might suppress 14-3-3 gamma expression. Analysis of the gamma promoter sequence revealed the presence of a p53 consensus binding motif and in vitro assays demonstrated that wild-type p53 bound to this motif when activated by ionizing radiation. Deletion of the p53 binding motif eliminated p53's ability to suppress 14-3-3gamma expression.CONCLUSION:Increased expression of 14-3-3gamma in lung cancer coincides with loss of functional p53. Hence, we propose that 14-3-3gamma's oncogenic activities cooperate with loss of p53 to promote lung tumorigenesis.
    EISSN
     1471-2407
    DOI
    10.1186/1471-2407-11-378
    Version
    Final published version
    Additional Links
    http://www.biomedcentral.com/1471-2407/11/378
    ae974a485f413a2113503eed53cd6c53
    10.1186/1471-2407-11-378
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