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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1995-12-19
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pubmed:abstractText |
Apoptotic cell death induced by cross-linking Fas receptor (FasR/CD95) has been investigated in human acute myelogenous leukemia (AML) cells. FasR-mediated growth inhibition and DNA fragmentation could be induced in certain cases of AML. Interestingly, when DNA synthesis and G1 -> S transition in the cell cycle were enhanced by interleukin-3 or granulocyte-macrophage colony-stimulating factor, Fas-insensitive blast cells acquired cellular susceptibility toward FasR-mediated growth inhibition. To further evaluate an association between the Fas-R-mediated action and a specific phase of the cell cycle, a FasR+ leukemic cell line, MML-1, was established from a patient with AML. The morphologic feature of dying cells and DNA fragmentation indicated that FasR cross-linking induced apoptotic cell death in MML-1 cells. Cell cycle arrest in G1A phase with the treatment of phorbol 12-myristate 13-acetate or thymidine rendered MML-1 cells resistant to FasR-mediated apoptosis without downregulation of surface FasR expression. However, S-phase arrest with 5-fluorouracil could neither enhance nor inhibit FasR-mediated apoptosis. Simultaneous DNA/RNA quantification analysis revealed the selective loss of cells in G1B compartment, accompanied by the increase of apoptotic nuclei in sub-G1 fraction. These findings suggested that FasR-mediated apoptotic signals could be transduced into cells in G1B compartment and G1A -> G1B transition might augment the induction of FasR-mediated apoptosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorouracil,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/Thymidine
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
86
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3848-60
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7579353-Acute Disease,
pubmed-meshheading:7579353-Antibodies, Monoclonal,
pubmed-meshheading:7579353-Antigens, CD95,
pubmed-meshheading:7579353-Apoptosis,
pubmed-meshheading:7579353-Cell Division,
pubmed-meshheading:7579353-Child,
pubmed-meshheading:7579353-Child, Preschool,
pubmed-meshheading:7579353-DNA, Neoplasm,
pubmed-meshheading:7579353-DNA Damage,
pubmed-meshheading:7579353-Fluorouracil,
pubmed-meshheading:7579353-G1 Phase,
pubmed-meshheading:7579353-Humans,
pubmed-meshheading:7579353-Leukemia, Myeloid,
pubmed-meshheading:7579353-Neoplastic Stem Cells,
pubmed-meshheading:7579353-RNA, Neoplasm,
pubmed-meshheading:7579353-Signal Transduction,
pubmed-meshheading:7579353-Tetradecanoylphorbol Acetate,
pubmed-meshheading:7579353-Thymidine,
pubmed-meshheading:7579353-Tumor Cells, Cultured
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pubmed:year |
1995
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pubmed:articleTitle |
Fas receptor (CD95)-mediated apoptosis is induced in leukemic cells entering G1B compartment of the cell cycle.
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pubmed:affiliation |
Department of Pediatrics, Mie University School of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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