Neuroblastoma is a childhood cancer, which spontaneously regresses. This has led to a search for agents that mimic this process. We show that both natural and synthetic ligands of PPARγ (peroxisome-proliferator-activated receptor γ) inhibit the growth of neuroblastoma cells in vitro. The degree of PPAR activation was attenuated however in the presence of the retinoblastoma protein. Addition of trichostatin A, a histone deacetylase inhibitor, abolished retinoblastoma protein repression of PPAR activity. Moreover, enhanced growth inhibition was observed when neuroblastoma cells were treated with a PPARγ ligand and a histone deacetylase inhibitor, suggesting a combination therapy to treat neuroblastoma might prove more effective than using either agent alone.
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November 2004
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Conference Article|
October 26 2004
Regulation of cellular processes by PPARγ ligands in neuroblastoma cells is modulated by the level of retinoblastoma protein expression
V.C. Emmans;
V.C. Emmans
*Development and Cell Biology, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, U.K.
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H.A. Rodway;
H.A. Rodway
*Development and Cell Biology, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, U.K.
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A.N. Hunt;
†Department of Child Health, University of Southampton, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, U.K.
1To whom correspondence should be addressed (email kal@soton.ac.uk).
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K.A. Lillycrop
K.A. Lillycrop
1
*Development and Cell Biology, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, U.K.
1To whom correspondence should be addressed (email kal@soton.ac.uk).
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Publisher: Portland Press Ltd
Received:
July 23 2004
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2004 The Biochemical Society
2004
Biochem Soc Trans (2004) 32 (5): 840–842.
Article history
Received:
July 23 2004
Citation
V.C. Emmans, H.A. Rodway, A.N. Hunt, K.A. Lillycrop; Regulation of cellular processes by PPARγ ligands in neuroblastoma cells is modulated by the level of retinoblastoma protein expression. Biochem Soc Trans 1 November 2004; 32 (5): 840–842. doi: https://doi.org/10.1042/BST0320840
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