Regulation of cellular processes by PPAR? ligands in neuroblastoma cells is modulated by the level of retinoblastoma protein expression
Regulation of cellular processes by PPAR? ligands in neuroblastoma cells is modulated by the level of retinoblastoma protein expression
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 PPAR? (peroxisome-proliferator-activated receptor ?) 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 PPAR? ligand and a histone deacetylase inhibitor, suggesting a combination therapy to treat neuroblastoma might prove more effective than using either agent alone.
cancer, neuroblastoma cells, nuclear receptor, peroxisome-proliferator-activated receptor ? (ppar?), retinoblastoma protein, transcription
840-842
Emmans, V.C.
499de643-01c3-4e6f-a4b2-779d51334f36
Rodway, H.A.
358861f5-2ea9-4612-ae8a-998376399d9a
Hunt, A.N.
95a3e223-da96-40e7-b47d-27dce014e305
Lillycrop, K.A.
eeaaa78d-0c4d-4033-a178-60ce7345a2cc
2004
Emmans, V.C.
499de643-01c3-4e6f-a4b2-779d51334f36
Rodway, H.A.
358861f5-2ea9-4612-ae8a-998376399d9a
Hunt, A.N.
95a3e223-da96-40e7-b47d-27dce014e305
Lillycrop, K.A.
eeaaa78d-0c4d-4033-a178-60ce7345a2cc
Emmans, V.C., Rodway, H.A., Hunt, A.N. and Lillycrop, K.A.
(2004)
Regulation of cellular processes by PPAR? ligands in neuroblastoma cells is modulated by the level of retinoblastoma protein expression.
Biochemical Society Transactions, 32, .
Abstract
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 PPAR? (peroxisome-proliferator-activated receptor ?) 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 PPAR? 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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Published date: 2004
Keywords:
cancer, neuroblastoma cells, nuclear receptor, peroxisome-proliferator-activated receptor ? (ppar?), retinoblastoma protein, transcription
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Local EPrints ID: 27039
URI: http://eprints.soton.ac.uk/id/eprint/27039
ISSN: 0300-5127
PURE UUID: cae0f30d-074b-46b3-8e05-fcc5d6762eb7
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Date deposited: 26 Apr 2006
Last modified: 23 Jul 2022 01:39
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Author:
V.C. Emmans
Author:
H.A. Rodway
Author:
A.N. Hunt
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