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Department of Biochemistry, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4–41 Ebara, Shinagawa, Tokyo 142-8501, Japan

(Requests for offprints should be addressed to M Watanabe; Email: masatada{at}hoshi.ac.jp)

We investigated the effects of epidermal growth factor (EGF) and prostaglandins (PG) on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells. EGF significantly increased aromatase activity and CYP19 gene transcript in NCI-H295R cells. Exon PII was selected from among several tissue-specific exon I regions. Promoter II that abuts on exon PII was activated by EGF. PGE₂ also significantly increased aromatase activity, CYP19 gene transcript, and promoter II activity. The results of experiments using protein kinase (PK) inhibitors suggest that the cAMP–PKA signaling pathway is involved in the up-regulation of aromatase expression by EGF. PGE₂ activated promoter II activity in 4 h, while12 h was required for its activation by EGF. In addition, PGE₂ was secreted from NCI-H295R cells in response to EGF. Selective agonists for prostaglandin receptors EP₁ and EP₂ significantly increased aromatase activity, which was decreased by the corresponding antagonists. Finally, antagonists for EP₁ and EP₂ inhibited the up-regulation of aromatase expression following EGF. These results suggest that PGE₂ secondarily acts as an autocrine signal in the up-regulation of aromatase expression by EGF in NCI-H295R cells.

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