Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1995-12-19
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3848-60
pubmed:dateRevised
2007-11-15
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
pubmed:year
1995
pubmed:articleTitle
Fas receptor (CD95)-mediated apoptosis is induced in leukemic cells entering G1B compartment of the cell cycle.
pubmed:affiliation
Department of Pediatrics, Mie University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't