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Transcription of the protein kinase C-delta gene is activated by JNK through c-Jun and ATF2 in response to the anticancer agent doxorubicin

Authors
Min, Byong WookKim, Chang GunKo, JesangLim, YoonghoLee, Young HanShin, Soon Young
Issue Date
31-Dec-2008
Publisher
NATURE PUBLISHING GROUP
Keywords
activating transcription factor 2; apoptosis; doxorubicin; JNK mitogen-activated protein kinases; protein kinase C-delta; proto-oncogene proteins c-jun
Citation
EXPERIMENTAL AND MOLECULAR MEDICINE, v.40, no.6, pp.699 - 708
Indexed
SCIE
SCOPUS
KCI
Journal Title
EXPERIMENTAL AND MOLECULAR MEDICINE
Volume
40
Number
6
Start Page
699
End Page
708
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/16622
DOI
10.3858/emm.2008.40.6.699
ISSN
1226-3613
Abstract
Expression of protein kinase C-delta (PKC delta) is up-regulated by apoptosis-inducing stimuli. However, very little is known about the signaling pathways that control PKC delta gene transcription. In the present study, we demonstrate that JNK stimulates PKC delta gene expression via c-Jun and ATF2 in response to the anticancer agent doxorubicin (DXR) in mouse lymphocytic leukemia L1210 cells. Luciferase reporter assays showed that DXR-induced activation of the PKC8 promoter was enhanced by ectopic expression of JNK1, c-Jun, or ATF2, whereas it was strongly reduced by expression of dominant negative JNK1 or by treatment with the JNK inhibitor SP600125. Furthermore, point mutations in the core sequence of the c-Jun/ATF2 binding site suppressed DXR-induced activation of the PKC8 promoter. Our results suggest an additional role for a JNK signaling cascade in DXR-induced PKC delta gene expression.
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Min, Byung Wook
Guro Hospital (Department of Colon and Rectal Surgery, Guro Hospital)
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