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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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| Published in: | Cellular and molecular life sciences : CMLS 2002-11, Vol.59 (11), p.2004-2012 |
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| container_end_page | 2012 |
| container_issue | 11 |
| container_start_page | 2004 |
| container_title | Cellular and molecular life sciences : CMLS |
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| creator | Fimognari, C Nüsse, M Berti, F Iori, R Cantelli-Forti, G Hrelia, P |
| description | 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. |
| doi_str_mv | 10.1007/PL00012523 |
| format | article |
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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.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/PL00012523</identifier><identifier>PMID: 12530531</identifier><language>eng</language><publisher>Switzerland: Springer Nature B.V</publisher><subject>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</subject><ispartof>Cellular and molecular life sciences : CMLS, 2002-11, Vol.59 (11), p.2004-2012</ispartof><rights>Birkhäuser Verlag 2002</rights><rights>Birkhäuser Verlag, 2002 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-2b1445b4f65734fa50284c8435bf8b7ff20949f3ac8115eef47a30ea4864a1603</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337518/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337518/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12530531$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fimognari, C</creatorcontrib><creatorcontrib>Nüsse, M</creatorcontrib><creatorcontrib>Berti, F</creatorcontrib><creatorcontrib>Iori, R</creatorcontrib><creatorcontrib>Cantelli-Forti, G</creatorcontrib><creatorcontrib>Hrelia, P</creatorcontrib><title>Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell Mol Life Sci</addtitle><description>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.</description><subject>Anticarcinogenic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Chemotherapy</subject><subject>Cyclin D2</subject><subject>Cyclin D3</subject><subject>Cyclin-Dependent Kinase 4</subject><subject>Cyclin-Dependent Kinase 6</subject><subject>Cyclin-Dependent Kinases - genetics</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Cyclins - genetics</subject><subject>Cyclins - metabolism</subject><subject>Humans</subject><subject>Isothiocyanates</subject><subject>Leukemia</subject><subject>Lymphocytes</subject><subject>Molecular biology</subject><subject>Proto-Oncogene Proteins - 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| 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 |
| title | Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes |
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