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Sulforaphane induces cytotoxicity and lysosome- and mitochondria-dependent cell death in colon cancer cells with deleted p53
E. Rudolf, M. Cervinka
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- antikarcinogenní látky toxicita MeSH
- časové faktory MeSH
- delece genu MeSH
- fyziologický stres účinky léků MeSH
- HCT116 buňky MeSH
- lidé MeSH
- lyzozomy účinky léků metabolismus MeSH
- MAP kinasa-kinasa 4 genetika metabolismus MeSH
- mitochondrie účinky léků metabolismus MeSH
- nádorový supresorový protein p53 genetika metabolismus MeSH
- nádory tračníku genetika metabolismus prevence a kontrola MeSH
- poškození DNA účinky léků MeSH
- proliferace buněk účinky léků MeSH
- protein X asociovaný s bcl-2 genetika metabolismus MeSH
- proteiny teplotního šoku genetika metabolismus MeSH
- regulace genové exprese u nádorů účinky léků MeSH
- thiokyanatany toxicita MeSH
- viabilita buněk účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Mechanisms and pathways responsible for cytotoxicity of sulforaphane (SF) in colon cancer cells with deleted p53 were investigated during 48 h of exposure. SF showed dose-dependent cytotoxicity and proapoptotic activity in the present model. In addition, in HCT-116 p53KO cells SF induced DNA damage with the subsequent cellular response and signaling not including p53 and caspase-2 pathways. Conversely, in SF-treated cells JNK was activated which led to an early lysosomal membrane permeabilization, release of cathepsin B and D and activation of Bid by specific cleavage. Concomitantly, the expression of Bax increased in the presence of JNK-mediated Bcl-2 inhibition which was followed by mitochondrial release of cytochrome c and activation of apoptosis. These results suggest that SF may be useful as a chemopreventive agent in colon cancer with inactivated or lost p53.
Citace poskytuje Crossref.org
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- $a Mechanisms and pathways responsible for cytotoxicity of sulforaphane (SF) in colon cancer cells with deleted p53 were investigated during 48 h of exposure. SF showed dose-dependent cytotoxicity and proapoptotic activity in the present model. In addition, in HCT-116 p53KO cells SF induced DNA damage with the subsequent cellular response and signaling not including p53 and caspase-2 pathways. Conversely, in SF-treated cells JNK was activated which led to an early lysosomal membrane permeabilization, release of cathepsin B and D and activation of Bid by specific cleavage. Concomitantly, the expression of Bax increased in the presence of JNK-mediated Bcl-2 inhibition which was followed by mitochondrial release of cytochrome c and activation of apoptosis. These results suggest that SF may be useful as a chemopreventive agent in colon cancer with inactivated or lost p53.
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