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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1-2
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pubmed:dateCreated |
1995-3-20
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pubmed:abstractText |
The induction of apoptosis following topoisomerase inhibitors proceeds in at least three distinct steps: (1) induction of cleavable complexes (potentially lethal damage), (2) topoisomerase-induced DNA damage, and (3) a presently unknown sequence of events that must either lead to cell cycle arrest (G2-block, differentiation) or apoptosis. DNA degradation provides a convenient way to quantify apoptosis in HL-60 cells. Extensive apoptosis can be induced rapidly in undifferentiated HL-60 cells without prevention by cycloheximide or actinomycin D. Therefore, HL-60 cells appear to express constitutively the apoptotic machinery that may be kept under control of a yet unknown repressor. The absence of the tumor suppressor p53 and the presence of bcl-2 are in contrast with the sensitivity of these cells to apoptosis. Agents that modify chromatin structure (zinc, poly[ADPribose] inhibitors, spermine) can block DNA fragmentation without affecting cell survival. By contrast macrophage-like differentiation by phorbol esters suppresses apoptosis without affecting topoisomerase-induced DNA damage. Better understanding of the apoptotic regulation in the widely used and characterized HL-60 cell line should allow the identification of new mechanisms and parameters of cellular sensitivity and resistance to the cytotoxic activity of anticancer agents.
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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,
http://linkedlifedata.com/resource/pubmed/chemical/Chromatin,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Topoisomerases, Type I,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Topoisomerases, Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoids,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Poly(ADP-ribose) Polymerases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Topoisomerase I Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Topoisomerase II Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1042-8194
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:geneSymbol |
bcl-2,
p53
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
21-32
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:7858500-Antineoplastic Agents,
pubmed-meshheading:7858500-Apoptosis,
pubmed-meshheading:7858500-Cell Cycle,
pubmed-meshheading:7858500-Cell Differentiation,
pubmed-meshheading:7858500-Chromatin,
pubmed-meshheading:7858500-DNA, Neoplasm,
pubmed-meshheading:7858500-DNA Damage,
pubmed-meshheading:7858500-DNA Topoisomerases, Type I,
pubmed-meshheading:7858500-DNA Topoisomerases, Type II,
pubmed-meshheading:7858500-Glucocorticoids,
pubmed-meshheading:7858500-Humans,
pubmed-meshheading:7858500-Leukemia, Promyelocytic, Acute,
pubmed-meshheading:7858500-Neoplasm Proteins,
pubmed-meshheading:7858500-Poly(ADP-ribose) Polymerases,
pubmed-meshheading:7858500-Proto-Oncogene Proteins,
pubmed-meshheading:7858500-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:7858500-Signal Transduction,
pubmed-meshheading:7858500-Topoisomerase I Inhibitors,
pubmed-meshheading:7858500-Topoisomerase II Inhibitors,
pubmed-meshheading:7858500-Tumor Cells, Cultured,
pubmed-meshheading:7858500-Tumor Suppressor Protein p53
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pubmed:year |
1994
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pubmed:articleTitle |
Apoptosis induced by DNA topoisomerase I and II inhibitors in human leukemic HL-60 cells.
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pubmed:affiliation |
Laboratory of Oncohematology, University of Medicine, Dijon, France.
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pubmed:publicationType |
Journal Article,
Review
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