계명대학교 의학도서관 Repository

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

Metadata Downloads
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.
공개 및 라이선스
  • 공개 구분공개
  • 엠바고Forever
파일 목록

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.