April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Positive Feedback Between p53 and PERP During Apoptosis Induction in Uveal Melanoma Cells
Author Affiliations & Notes
  • Natalie M. Hill
    Eye and Vision Science, Institute of Ageing and Chronic Disease,
    University of Liverpool, Liverpool, United Kingdom
  • Lyndsay Davies
    Eye and Vision Science, Institute of Ageing and Chronic Disease,
    University of Liverpool, Liverpool, United Kingdom
  • Dave Spiller
    Centre for Cell Imaging, Institute of Integrative Biology,
    University of Liverpool, Liverpool, United Kingdom
  • Mike White
    Centre for Cell Imaging, Institute of Integrative Biology,
    University of Liverpool, Liverpool, United Kingdom
  • Ian Grierson
    Eye and Vision Science, Institute of Ageing and Chronic Disease,
    University of Liverpool, Liverpool, United Kingdom
  • Luminita Paraoan
    Eye and Vision Science, Institute of Ageing and Chronic Disease,
    University of Liverpool, Liverpool, United Kingdom
  • Footnotes
    Commercial Relationships  Natalie M. Hill, None; Lyndsay Davies, None; Dave Spiller, None; Mike White, None; Ian Grierson, None; Luminita Paraoan, None
  • Footnotes
    Support  Supported by The Humane Research Trust, UK.
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 513. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Natalie M. Hill, Lyndsay Davies, Dave Spiller, Mike White, Ian Grierson, Luminita Paraoan; Positive Feedback Between p53 and PERP During Apoptosis Induction in Uveal Melanoma Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):513.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : We have previously shown that the expression of PERP (p53 apoptosis effector related to PMP-22), an apoptosis-specific effector of p53, triggers the death of uveal melanoma cells by apoptosis. The purpose of this study was to investigate the effect of increased PERP expression on the expression and subcellular localisation of its own upstream transcriptional regulator, p53.

Methods: : Fluorescent fusion protein constructs of PERP, p53 and MDM2, were used to transfect the human uveal melanoma cell line MEL202. Western blotting was used to detect the expression of green fluorescent protein-PERP fusion (GFP-PERP), p53 and MDM2. The subcellular localization of PERP, p53 and MDM2 fluorescent fusion proteins in transfected cells was analysed by confocal microscopy.

Results: : Significantly increased levels of p53 protein were observed in MEL202 cells expressing GFP-PERP compared with control cells, which was also accompanied by an increase in the levels of p53 negative regulator MDM2. Expression of GFP-PERP resulted in nuclear localization of MDM2-yellow fluorescent protein (MDM2-YFP) in 96.8% of co-transfected cells. In contrast, MDM2-YFP expression alone or in combination with GFP expression had additional diffuse cytoplasmic localization. In the absence of GFP-PERP expression, p53 fused to red fluorescent protein (p53-RFP) was localized primarily in the cytoplasm with low expression in the nucleus. However, following GFP-PERP expression, p53-RFP was localized predominantly in the nucleus in a significantly higher proportion of co-transfected cells.

Conclusions: : Our results show that PERP protein levels influence the protein levels of its own transcriptional regulator, p53. Additionally, PERP expression causes nuclear localization of p53 that is critical for its transcriptional function. Together, these results propose a novel role for PERP in enhancing p53 levels and reveal a potential new target for exploitation in the development of new therapeutic agents aimed at increasing the endogenous p53 protein pool in neoplastic cells.

Keywords: apoptosis/cell death • transcription factors • melanoma 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×