Source:http://linkedlifedata.com/resource/pubmed/id/17145055
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2007-1-12
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pubmed:abstractText |
Taxol is an anticancer drug that triggers apoptosis in a wide spectrum of cancers such as ovarian, breast, lung, head and neck, and bladder carcinoma by both caspase-dependent and -independent apoptosis mechanisms. However, the exact signaling pathways involved in taxol-induced apoptosis strongly depend on the cellular background and they are not completely established yet. In this study we demonstrate that taxol induces caspase-3-independent apoptosis in NIH3T3 cells by a calpain-mediated mechanism. Taxol treatment produced changes in the mitochondrial membrane potential (Delta Psi m) which could be responsible of Ca(2+) release from the mitochondria and the consequent calpain activation. Interestingly, we show that calpain produced proteolysis of caspase-3 and demonstrate that, accordingly, calpain inhibition increased taxol-induced apoptosis. In addition, we reveal that poly (ADP-ribose) polymerase (PARP) was processed by calpain in taxol-treated cells and by caspase-3 after calpain inhibition. In conclusion, these results demonstrate for the first time that calpain could play an important role modulating taxol-induced apoptosis. Further studies are needed to address the potentiality of inducing apoptosis by a combined use of taxol and calpain inhibitors in cells with increased calpain activity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, Phytogenic,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calpain,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine Proteinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Dipeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Paclitaxel,
http://linkedlifedata.com/resource/pubmed/chemical/calpain inhibitor III
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0014-4827
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
313
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
369-79
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pubmed:meshHeading |
pubmed-meshheading:17145055-Animals,
pubmed-meshheading:17145055-Antineoplastic Agents, Phytogenic,
pubmed-meshheading:17145055-Apoptosis,
pubmed-meshheading:17145055-Calcium,
pubmed-meshheading:17145055-Calpain,
pubmed-meshheading:17145055-Caspase 3,
pubmed-meshheading:17145055-Cysteine Proteinase Inhibitors,
pubmed-meshheading:17145055-Cytoplasm,
pubmed-meshheading:17145055-Dipeptides,
pubmed-meshheading:17145055-Membrane Potential, Mitochondrial,
pubmed-meshheading:17145055-Mice,
pubmed-meshheading:17145055-NIH 3T3 Cells,
pubmed-meshheading:17145055-Paclitaxel
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pubmed:year |
2007
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pubmed:articleTitle |
Calpain inhibition stimulates caspase-dependent apoptosis induced by taxol in NIH3T3 cells.
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pubmed:affiliation |
Servicio de Bioquímica-Investigación, Hospital Ramón y Cajal, Ctra Colmenar km 9,100, 28034 Madrid, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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