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rdf:type |
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lifeskim:mentions |
umls-concept:C0007600,
umls-concept:C0036667,
umls-concept:C0079419,
umls-concept:C0086418,
umls-concept:C0144576,
umls-concept:C0162638,
umls-concept:C0205263,
umls-concept:C0312418,
umls-concept:C0334227,
umls-concept:C0442805,
umls-concept:C1140680,
umls-concept:C1517345
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pubmed:issue |
1
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pubmed:dateCreated |
1998-7-8
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pubmed:abstractText |
Paclitaxel-induced cytotoxicity, cell cycle perturbation, and apoptosis were determined in a human ovarian cancer cell line expressing wt p53 (A2780) and in a subclone (A2780/E6) obtained upon transfection with the product of the E6 gene of the human papilloma virus HPV16. The inactivation of wt p53 in A2780/E6 was verified by measuring the inability of the clone to induce p53 and p21 expression after paclitaxel treatment. The p53-negative clone (A2780/E6) was approximately 50-fold more sensitive to paclitaxel than wt p53-expressing A2780 cells. This increased sensitivity was related to the ability of paclitaxel to induce a strong arrest of cells in the G2/M phase of the cell cycle in A2780/E6 but not in A2780 cells. This different cell cycle arrest was accompanied by increased frequency of paclitaxel-induced p53-independent apoptosis. Initial studies on proteases activation tend to exclude a direct role of ICE and CPP32 in the induction of apoptosis in these cells and show a paclitaxel-dependent increase in FLICE levels, whose biological relevance is however at present not defined.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, Phytogenic,
http://linkedlifedata.com/resource/pubmed/chemical/CASP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/DAPI,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Protein p21(ras),
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/Paclitaxel,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53,
http://linkedlifedata.com/resource/pubmed/chemical/oncogene protein E5, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0014-4827
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
241
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
96-101
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9633517-Antineoplastic Agents, Phytogenic,
pubmed-meshheading:9633517-Apoptosis,
pubmed-meshheading:9633517-Caspase 3,
pubmed-meshheading:9633517-Caspases,
pubmed-meshheading:9633517-Cell Death,
pubmed-meshheading:9633517-Cell Nucleus,
pubmed-meshheading:9633517-Cysteine Endopeptidases,
pubmed-meshheading:9633517-Female,
pubmed-meshheading:9633517-G2 Phase,
pubmed-meshheading:9633517-HL-60 Cells,
pubmed-meshheading:9633517-Humans,
pubmed-meshheading:9633517-Indoles,
pubmed-meshheading:9633517-Mitosis,
pubmed-meshheading:9633517-Oncogene Protein p21(ras),
pubmed-meshheading:9633517-Oncogene Proteins, Viral,
pubmed-meshheading:9633517-Ovarian Neoplasms,
pubmed-meshheading:9633517-Paclitaxel,
pubmed-meshheading:9633517-Recombinant Proteins,
pubmed-meshheading:9633517-Sensitivity and Specificity,
pubmed-meshheading:9633517-Transfection,
pubmed-meshheading:9633517-Tumor Cells, Cultured,
pubmed-meshheading:9633517-Tumor Suppressor Protein p53
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pubmed:year |
1998
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pubmed:articleTitle |
Inactivation of p53 in a human ovarian cancer cell line increases the sensitivity to paclitaxel by inducing G2/M arrest and apoptosis.
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pubmed:affiliation |
Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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