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Vol. 57, Issue 1, 153-161, January 2000
Department of Pharmacology, College of Medicine, National Cheng
Kung University, Tainan, Taiwan
The role of mitogen-activated protein kinase signaling and the
transcription factor c-Jun in epidermal growth factor (EGF)-induced expression of 12-lipoxygenase in human epidermoid carcinoma A431 cells
was studied. EGF increased the activation of extracellular signal-regulated kinase (ERK) and c-Jun amino terminal kinase (JNK) in
a time-dependent manner. Treatment of the cells with an
mitogen-activated protein kinase kinase inhibitor, PD098059 (30 µM), inhibited the EGF- and pSV2ras-induced expression of 12-lipoxygenase mRNA. Transfection of the cells with Ras, ERK2, Rac,
JNK dominant negative mutants pMMrasDN, K52R ERK2, RacN17, and mJNK all
inhibited the EGF-induced promoter activation of the 12-lipoxygenase
gene. EGF induced the expression of c-Jun and the activity of
transcription factor activator protein 1 in cells, and these
effects were blocked by the treatment with K52R ERK2 and mJNK.
Overexpression of c-Jun increased the expression of 12-lipoxygenase
mRNA and enzyme activity. Furthermore, the Sp1-binding sites in the
promoter region of the 12-lipoxygenase gene were requisite for c-Jun
response, which was similar to that previously observed in EGF
response. The results indicate that the EGF-induced expression of
12-lipoxygenase in A431 cells was mediated through the Ras-ERK and
Ras-Rac-JNK signal pathways. Subsequent induction of c-Jun led by ERK
and JNK activation was essential for this EGF response.
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