Document 0939
 DOCN  M9540939
 TI    Induction of ICAM-1 and LFA-3 by Tax1 of human T-cell leukemia virus
       type 1 and mechanism of down-regulation of ICAM-1 or LFA-1 in
       adult-T-cell-leukemia cell lines.
 DT    9504
 AU    Tanaka Y; Fukudome K; Hayashi M; Takagi S; Yoshie O; Shionogi Institute
       for Medical Science, Osaka, Japan.
 SO    Int J Cancer. 1995 Feb 8;60(4):554-61. Unique Identifier : AIDSLINE
       MED/95130292
 AB    The present study was undertaken to determine the role of HTLV-I TaxI in
       the up-regulation of ICAM-I and LFA-3 in human T cells transformed with
       HTLV-I and the mechanism of down-regulation of ICAM-I and LFA-I in
       ATL-derived cell lines. Induction of TaxI in a human T-cell line Jurkat
       carrying the TaxI gene under the metallothionein promoter led to
       increases in mRNA and surface expression of ICAM-I. The response of
       LFA-3 to TaxI induction was, on the other hand, relatively slow and
       weak, and might be indirect. Transactivation of the ICAM-I promoter by
       TaxI was further shown by co-transfection of a CAT reporter construct
       with the ICAM-I promoter and a plasmid expressing TaxI. The mechanism of
       down-regulation of ICAM-I or LFA-I in 4 ATL cell lines was next
       examined. ICAM-I mRNA was quite low in MT-I, but no genomic changes were
       found. The CAT reporter with the ICAM-I promoter was inactive in MT-I.
       Finally, combined treatment of MT-I with 5-azacytidine and IFN-gamma
       induced re-expression of ICAM-I. Collectively, (a) transcriptional
       factor(s) necessary for expression of ICAM-I gene may be repressed in
       MT-I through DNA methylation. Three other ATL cell lines (TL-OmI, H582,
       HuT102) were found to have little mRNA for the LFA-I beta chain (CD18).
       H582 and HuT102 were also negative for the LFA-I alpha chain (CDIIa)
       mRNA. No genomic changes were found, and a CAT reporter gene with the
       CD18 promoter was inactive in the 3 of them, again suggesting lack of
       (a) transcriptional factor(s) necessary for CD18 expression.
 DE    Antigens, CD/BIOSYNTHESIS  Base Sequence  Blotting, Northern  Blotting,
       Southern  Cell Adhesion Molecules/*BIOSYNTHESIS/GENETICS  Cell Line,
       Transformed/METABOLISM  Chloramphenicol Acetyltransferase/GENETICS
       Down-Regulation (Physiology)  DNA Primers  DNA, Viral/GENETICS  Gene
       Expression Regulation, Neoplastic  Gene Expression Regulation, Viral
       Gene Products, tax/METABOLISM  Genes, tat/*PHYSIOLOGY  Genes, Reporter
       Human  HTLV-I/GENETICS/*PHYSIOLOGY  Intercellular Adhesion
       Molecule-1/BIOSYNTHESIS  Leukemia, T-Cell/METABOLISM/*VIROLOGY
       Lymphocyte Function-Associated Antigen-1/BIOSYNTHESIS  Membrane
       Glycoproteins/BIOSYNTHESIS  Methylation  Molecular Sequence Data
       Promoter Regions (Genetics)  Repressor Proteins/METABOLISM
       T-Lymphocytes/*METABOLISM/VIROLOGY  Trans-Activation (Genetics)  Tumor
       Cells, Cultured/METABOLISM  Up-Regulation (Physiology)  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).