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KMID : 0620920080400060699
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Experimental & Molecular Medicine
2008 Volume.40 No. 6 p.699 ~ p.708
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Transcription of the protein kinase C-d gene is activated by JNK through c-Jun and ATF2 in response to the anticancer agent doxorubicin
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Min Byong-Wook
Ko Je-Sang
Lim Yoong-Ho
Kim Chang-Gun
Lee Young-Han
Shin Soon-Young
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Abstract
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Expression of protein kinase C-d (PKCd) is up-regulated by apoptosis-inducing stimuli. However, very little is known about the signaling pathways that control PKCd gene transcription. In the present study, we demonstrate that JNK stimulates PKCd 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 PKCd 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 PKCd promoter. Our results suggest an additional role for a JNK signaling cascade in DXR-induced PKCd gene expression.
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KEYWORD
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activating transcription factor 2, apoptosis, doxorubicin, JNK mitogen-activated protein kinases, protein kinase C-δ , proto-oncogene proteins c-jun
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