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Inhibition of both mesothelioma cell growth and Cdk4 activity following treatment with a TATp16INK4a peptide

Sandra P Frizelle1, Marian G Kratzke, Richard R Carreon

  • 1Research Service, Minneapolis Veterans Affairs Medical Center, Minneapolis, MN 55417, USA.

Anticancer Research
|April 4, 2008
PubMed
Abstract

Insights

Reintroducing p16INK4a protein into mesothelioma cells using the TAT delivery system induced cell death and cell cycle arrest. This suggests a potential new therapy for mesothelioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Mesothelioma is often associated with the disruption of the 9p21 locus.
  • This disruption results in the loss of critical tumor suppressor gene products, p16INK4a and p14ARF.

Purpose of the Study:

  • To investigate the potential of reexpressing p16INK4a in mesothelioma cells.
  • To determine if the TAT delivery system can facilitate p16INK4a protein transduction and induce mesothelioma cell death.

Main Methods:

  • A synthetic TATp16INK4a peptide was created using the HIV TAT protein transduction domain.
  • This peptide and a control were introduced into mesothelioma cells both in vitro and in vivo.
  • Assays were performed to measure Cdk4 inhibition, cell cycle arrest, and cell death.

Main Results:

  • Treatment with TATp16INK4a peptide led to significant mesothelioma cell death within 48 hours.
  • Apoptosis and G1 cell cycle arrest were observed in treated cells.
  • Transient hypophosphorylation of pRb and similar effects were noted in mesothelioma xenografts.

Conclusions:

  • Reexpression of p16INK4a via the TAT delivery system shows promise for mesothelioma treatment.
  • Therapeutic strategies involving TATp16INK4a peptide or small molecule mimetics could be effective.

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