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Originally published In Press as doi:10.1074/jbc.M206550200 on October 8, 2002

J. Biol. Chem., Vol. 277, Issue 50, 48234-48240, December 13, 2002
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UV Stimulation of Nucleophosmin/B23 Expression Is an Immediate-early Gene Response Induced by Damaged DNA*

Ming H. WuDagger § and Benjamin Y. M. Yung§

From the Dagger  Graduate Institute of Pharmacology, National Yang Ming University, Taipei 112, Taiwan, Republic of China; and § Cancer Biochemistry Laboratory, Department of Pharmacology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-San, Tao-Yuan 333, Taiwan, Republic of China

Nucleophosmin/B23 (NPM/B23), a nucleolar protein, was rapidly up-regulated after UV irradiation (at 254 nm; 30 J/m2) in NIH 3T3 cells and HeLa/S3 cells. Levels of NPM/B23 mRNA peaked 45-60 min after UV treatment and returned to baseline by 12 h. Transcription inhibitor actinomycin D (5 µg/ml) prevented the UV-induced increase of NPM/B23 mRNA, suggesting that UV induction of NPM/B23 was mediated at the transcriptional level. Moreover, UV-induced NPM/B23 expression was super-induced by cycloheximide (20 µg/ml), which was characteristic of immediate-early gene response. The transcriptional activation of NPM/B23 by UV was also confirmed by NPM/B23 promoter activity assay. Thymine dinucleotide, mimicking the effects of UV-induced DNA damage, was able to trigger NPM/B23 expression in the absence of genomic DNA damage. UV-induced activation of NPM/B23 promoter could not be blocked by UV-inducible pathway inhibitors, such as those of growth factor tyrosine kinase, mitogen-activated protein kinase, AP-1, NF-kappa B, and DNA-dependent kinase. Our results indicate that UV stimulation of NPM/B23 expression may be mediated through a novel UV-inducible pathway and is an immediate-early gene response induced by damaged DNA. Induction of immediate-early gene is an initial step in the regulation of cellular and genomic responses to external stimuli. Our results thus provide important evidence for an involvement of NPM/B23 in the acute response of mammalian cells to environmental stress.

* This work was supported by Chang Gung Memorial Hospital Research Funding Grant CMRP 997III, National Science Council (R.O.C) Grant NSC90-2315-B-182-001, and National Research Institute of Heath Council (R.O.C) Grant NHRI-EX91-8935SL.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Fax: 886-3-328-2015; E-mail: byung@mail.cgu.edu.tw.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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