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AP2 transcription factor induces apoptosis in retinoblastoma cells

Xiaodong Li1, Darryl D Glubrecht, Roseline Godbout

  • 1Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, Alberta, T6G 1Z2 Canada.

Genes, Chromosomes & Cancer
|July 8, 2010
PubMed

Insights

Loss of RB1 gene function in retinoblastoma inactivates TFAP2A and TFAP2B. This may lead to retinoblastoma tumor formation by preventing cell differentiation in the retina.

Area of Science:

  • Ophthalmology
  • Genetics
  • Cell Biology

Background:

  • Retinoblastoma is caused by RB1 gene inactivation.
  • Chromosome abnormalities, particularly extra copies of 6p, are common in retinoblastoma.
  • RB protein interacts with TFAP2 transcription factors.

Purpose of the Study:

  • Investigate the role of TFAP2A and TFAP2B in retinoblastoma.
  • Determine the relationship between RB1 gene function and TFAP2A/TFAP2B expression.
  • Explore the potential of TFAP2A and TFAP2B as therapeutic targets.

Main Methods:

  • Analysis of TFAP2A and TFAP2B expression in human retina and retinoblastoma.
  • Detection of TFAP2A RNA and protein, and TFAP2B RNA and protein.
  • Transfection of retinoblastoma cells with TFAP2A and TFAP2B expression constructs.

Main Results:

  • TFAP2A and TFAP2B are expressed in retinal amacrine and horizontal cells.
  • Most retinoblastoma cell lines and tumors lack TFAP2A protein and TFAP2B RNA/protein.
  • TFAP2A and TFAP2B expression induces apoptosis and inhibits proliferation in retinoblastoma cells.

Conclusions:

  • Loss of RB1 gene function in retinoblastoma leads to TFAP2A and TFAP2B inactivation.
  • TFAP2A and TFAP2B dysfunction may contribute to retinoblastoma development.
  • Inability to differentiate along amacrine/horizontal cell lineages might underlie retinoblastoma formation.

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