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12-O-tetradecanoyl phorbol 13-acetate induces the expression of B7-DC, -H1, -H2, and -H3 in K562 cells

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Affiliated Author(s)
장병철김상표황진복백원기서민호서성일문교철
Alternative Author(s)
Jang, Byeong ChurlKim, Sang PyoHwang, Jin BokBaek, Won KiSuh, Min HoSuh, Seong IlMun, Kyo Cheol
Journal Title
International Journal of Oncology
ISSN
1019-6439
Issued Date
2007
Abstract
. Induction of the B7 family molecules by 12-Otetradecanoyl
phorbol 13-acetate (TPA) has been reported,
however, the mechanism by which TPA up-regulates these
molecules remains poorly understood. In this study, the
expression of B7-DC, -H1, -H2, and -H3 in response to TPA
was markedly induced in K562 cells. TPA also induced
activation of ERK, p38 mitogen-activated protein kinase
(MAPK), JNK, phosphatidylinositol-3-kinase (PI-3K), or
nuclear factor (NF)-κB. Pre-treatments with protein kinase
C (PKC) inhibitors significantly inhibited TPA-induced
expression of B7-DC, -H1, -H2, and -H3 mRNA as well as
TPA-induced phosphorylation of ERK, p38 MAPK, JNK,
and PI-3K. TPA-induced expression of B7-DC, -H1, -H2, and
-H3 mRNA was abrogated by pre-treatments with inhibitors
of ERK and p38 MAPK. However, inhibition of PI-3K and
JNK only caused decrease of TPA-induced B7-DC mRNA
and B7-H3 mRNA, respectively. TPA-induced degradation
of IκB-α was markedly abrogated by treatments with PKC
inhibitors, but not by treatments with inhibitors of ERK,
p38 MAPK, JNK, or PI-3K. NF-κB inhibitors significantly
attenuated the expression of B7-DC, -H1, -H2, and -H3 mRNA
in response to TPA. These results suggest that TPA induces
the expression of B7-DC, -H1, -H2, and -H3 mRNA in K562
cells via activation of PKC, ERK, p38 MAPK, and NF-κB.
Distinctly, the expression of B7-DC mRNA and -H3 mRNA
in response to TPA is also PI-3K- and JNK-dependent,
respectively.
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