Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes

Despite experimental evidence that sulforaphane can exert chemopreventive effects, whether these effects are specific for neoplastic cells is not known. Following our previous demonstration that sulforaphane induces cell cycle arrest and apoptosis in human T lymphoblastoid Jurkat leukemia cells and...

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Bibliographic Details
Published in:Cellular and molecular life sciences : CMLS 2002-11, Vol.59 (11), p.2004-2012
Main Authors: Fimognari, C, Nüsse, M, Berti, F, Iori, R, Cantelli-Forti, G, Hrelia, P
Format: Article
Language:English
Subjects:
Anticarcinogenic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
bcl-2-Associated X Protein
Cell cycle
Cell Cycle - drug effects
Chemotherapy
Cyclin D2
Cyclin D3
Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinase 6
Cyclin-Dependent Kinases - genetics
Cyclin-Dependent Kinases - metabolism
Cyclins - genetics
Cyclins - metabolism
Humans
Isothiocyanates
Leukemia
Lymphocytes
Molecular biology
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-bcl-2 - genetics
Proto-Oncogene Proteins c-bcl-2 - metabolism
Sulfoxides
T cell receptors
T-Lymphocytes - cytology
T-Lymphocytes - drug effects
T-Lymphocytes - metabolism
Thiocyanates - pharmacology
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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Summary:Despite experimental evidence that sulforaphane can exert chemopreventive effects, whether these effects are specific for neoplastic cells is not known. Following our previous demonstration that sulforaphane induces cell cycle arrest and apoptosis in human T lymphoblastoid Jurkat leukemia cells and increases p53 and bax protein expression, we tested sulforaphane on non-transformed phytohemagglutinin-stimulated human lymphocytes. Here, we demonstrate that sulforaphane arrested cell cycle progression in G, phase, through a decrease in the protein expression of cyclin D3. Moreover, sulforaphane induced apoptosis (and also necrosis), mediated by an increase in the expression of p53. These findings suggest that sulforaphane is a growth modulator for T cells. Our in vitro evidence that sulforaphane is active and even cytotoxic in normal as well as transformed lymphocytes raises important questions regarding its suitability for cancer chemoprevention.
ISSN:1420-682X
1420-9071
DOI:10.1007/PL00012523