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First published on July 20, 2006; DOI: 10.1124/mol.106.024810

0026-895X/06/7004-1443-1453$20.00
Mol Pharmacol 70:1443-1453, 2006

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Ras-Dependent Recruitment of c-Myc for Transcriptional Activation of Nucleophosmin/B23 in Highly Malignant U1 Bladder Cancer Cells

Chun-Wei Yeh, Sheng-Shun Huang, Ru-Ping Lee, and Benjamin Yat-Ming Yung

Cancer Biochemistry Laboratory, Department of Pharmacology, College of Medicine, Chang Gung University, Taiwan, Republic of China

U1 bladder cancer cells of high malignancy exhibited higher proliferation capacity than U4 premalignant cells. Higher expression of Ras, c-Myc, and nucleophosmin/B23 and greater c-Myc transactivation and nucleophosmin/B23 promoter activities were detected in U1 cells compared with U4 cells. Moreover, c-Myc and nucleophosmin/B23 were increased in U1 but not in U4 cells upon serum stimulation from quiescence. Likewise, only in U1 cells could serum stimulate transcriptional activity of nucleophosmin/B23 promoter and c-Myc response element. The increase of nucleophosmin/B23 promoter activity could be abrogated by mitogen-activated protein kinase/extracellular signal-regulated kinase activating kinase inhibitor and was associated with recruitment of c-Myc to the promoter. U1 cells constitutively expressing dominant-negative Ras reduced the levels of Ras, nucleophosmin/B23, and p-ERK, and consequently abolished the serum-induced up-regulation of nucleophosmin/B23 promoter activity and c-Myc promoter recruitment. Our results indicate that Ras and c-Myc play important roles in the up-regulation of nucleophosmin/B23 during proliferation of cells associated with a high degree of malignancy, thus outlining a signaling cascade involving these factors in the cancer cells.

Received March 22, 2006; accepted July 20, 2006

Address correspondence to: Dr. Benjamin Yat-Ming Yung, Cancer Bio-chemistry Laboratory, Department of Pharmacology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-San, Tao-Yuan 333, Taiwan, R.O.C. E-mail: byung{at}mail.cgu.edu.tw






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