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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-1-10
pubmed:abstractText
Retinoic acid (RA) has been used to induce the regression of refractory T-cell lymphoma. In vitro and in vivo studies have shown that RA exerts this effect through the induction of apoptosis. This study was designed to investigate the molecular pathway of RA-induced apoptosis in T-lymphoma cell lines.RA-induced apoptosis was verified by morphology, flow cytometry, and DNA ladder analysis. Differential display method using a combination of 12 poly(A)-anchored primers and 20 arbitrary primers was adopted for gene cloning. Total RNAs were extracted from H9 cell line at 0, 6, 12, and 24 hours after All-trans RA (ATRA) treatment and the serial expression patterns of the candidate fragments were recognized. The cloned gene fragments were then analyzed and confirmed by Northern blot analysis on H9 and SR786 cell lines.ATRA-induced apoptosis of T-cell lymphoma was protein synthesis-dependent. The execution or irreversible phase of apoptosis appeared to occur at 6-12 hours of RA treatment. Among the 60,000 arbitrarily displayed bands, 25 of 250 candidate fragments were selected for further cloning and sequencing. A total of 14 clones could be matched to known genes and were categorized into four groups: A) transcription factors: prothymosin, CA150, p78 serine/threonine kinase, IL-1beta-stimulating gene, glucocorticoid receptor, MLN64/CAB1, gastrin-binding protein, and polypeptide from glioblastoma; B) chaperone: 90 kDa heat shock protein; C) ion channel: chloride channel protein 3; and D) cytoskeleton: cytovillin2/ezrin and vimentin. Another two clones of genes were of unrecognized functions. The remaining 11 clones belonged to unmatched or novel genes. The expression of these genes varied, either upregulated or downregulated, in response to ATRA treatment.RA-induced apoptosis may involve a cascade of genes that are related to transcription regulation, stress response, housekeeping, and the execution of apoptosis. The clarification of the RA-induced apoptotic pathway will help us to understand the molecular mechanism of cancer differentiation agents.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0301-472X
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1441-50
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11146166-Apoptosis, pubmed-meshheading:11146166-Blotting, Northern, pubmed-meshheading:11146166-Chloride Channels, pubmed-meshheading:11146166-Cloning, Molecular, pubmed-meshheading:11146166-Cytoskeletal Proteins, pubmed-meshheading:11146166-DNA, pubmed-meshheading:11146166-DNA Fragmentation, pubmed-meshheading:11146166-Flow Cytometry, pubmed-meshheading:11146166-HSP90 Heat-Shock Proteins, pubmed-meshheading:11146166-Humans, pubmed-meshheading:11146166-Kinetics, pubmed-meshheading:11146166-Lymphoma, T-Cell, pubmed-meshheading:11146166-Phosphoproteins, pubmed-meshheading:11146166-Polymerase Chain Reaction, pubmed-meshheading:11146166-Sequence Alignment, pubmed-meshheading:11146166-Sequence Analysis, DNA, pubmed-meshheading:11146166-Transcription Factors, pubmed-meshheading:11146166-Tretinoin, pubmed-meshheading:11146166-Tumor Cells, Cultured, pubmed-meshheading:11146166-Vimentin
pubmed:year
2000
pubmed:articleTitle
Retinoic acid-induced apoptotic pathway in T-cell lymphoma: Identification of four groups of genes with differential biological functions.
pubmed:affiliation
Graduate Institute of Pathology, National Taiwan University Medical School, Taipei, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't