TY - JOUR
T1 - A human T lymphotropic virus type I (HTLV-I) long terminal repeat-directed antisense c-myc construct with an Epstein-Barr virus replicon vector inhibits cell growth in a HTLV-I-transformed human T cell line
AU - Fujita, Masatoshi
AU - Shiku, Hiroshi
N1 - Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1993/5/3
Y1 - 1993/5/3
N2 - A panel of EB virus replicon-based vectors was constructed to examine the relative utility of four distinct eukaryotic promoters for high-level gene expression in a HTLV-I-transformed human T cell line, HUT102. We found that HTLV-I LTR, which is trans-activated by the viral tax protein, was most suited for EBV vector-based stable gene expression in it. We prepared a HTLV-I LTR-directed antisense c-myc construct with an EBV vector. This antisense plasmid suppressed c-myc expression and inhibited growth of HUT102 cells in vitro with unaltered expression of tax. Non-specific plasmid toxicity was excluded by showing that the antisense construct had little effect on growth and c-myc expression of HTLV-I-negative Jurkat T cells, in which the viral LTR is expected to be less active. Our results indicate that c-myc may play an important role in the deregulated growth of HTLV-I-transformed T cells.
AB - A panel of EB virus replicon-based vectors was constructed to examine the relative utility of four distinct eukaryotic promoters for high-level gene expression in a HTLV-I-transformed human T cell line, HUT102. We found that HTLV-I LTR, which is trans-activated by the viral tax protein, was most suited for EBV vector-based stable gene expression in it. We prepared a HTLV-I LTR-directed antisense c-myc construct with an EBV vector. This antisense plasmid suppressed c-myc expression and inhibited growth of HUT102 cells in vitro with unaltered expression of tax. Non-specific plasmid toxicity was excluded by showing that the antisense construct had little effect on growth and c-myc expression of HTLV-I-negative Jurkat T cells, in which the viral LTR is expected to be less active. Our results indicate that c-myc may play an important role in the deregulated growth of HTLV-I-transformed T cells.
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U2 - 10.1016/0014-5793(93)81101-5
DO - 10.1016/0014-5793(93)81101-5
M3 - Article
C2 - 8387025
AN - SCOPUS:0027467192
VL - 322
SP - 15
EP - 20
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 1
ER -