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Molecular and Cellular Biology, August 2008, p. 4829-4842, Vol. 28, No. 15
0270-7306/08/$08.00+0     doi:10.1128/MCB.00175-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The Activated Notch1 Receptor Cooperates with {alpha}-Enolase and MBP-1 in Modulating c-myc Activity{triangledown}

Kai-Wen Hsu,1,2 Rong-Hong Hsieh,3 Yan-Hwa Wu Lee,4 Chi-Hong Chao,4 Kou-Juey Wu,4 Min-Jen Tseng,5 and Tien-Shun Yeh1*

Department of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan,1 Graduate Institute of Medical Sciences, College of Medicine,2 Graduate Institute of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan,3 Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 112, Taiwan,4 Department of Life Science, National Chung Cheng University, Chia-Yi 621, Taiwan5

Received 3 February 2008/ Returned for modification 7 March 2008/ Accepted 9 May 2008

The Notch signal pathway plays multifaceted roles to promote or suppress tumorigenesis. The Notch1 receptor intracellular domain (N1IC), the activated form of the Notch1 receptor, activates the c-myc proto-oncogene. The complex of N1IC and transcription factor YY1 binds to the human c-myc promoter to enhance c-myc expression in a CBF1-independent manner. Here we demonstrated that N1IC interacted with the c-Myc-regulating proteins {alpha}-enolase and c-myc promoter binding protein 1 (MBP-1). Both {alpha}-enolase and MBP-1 suppressed the N1IC-enhanced activity of the c-myc promoter in a CBF1-independent manner. The YY1 response element in front of the P2 c-myc promoter was essential and sufficient for the modulation of c-myc by N1IC and {alpha}-enolase or MBP-1. Furthermore, N1IC, YY1, and {alpha}-enolase or MBP-1 but not CBF1 bound to the c-myc promoter through associating with the YY1 response element. Hemin-induced erythroid differentiation was suppressed by N1IC in K562 cells. This suppression was relieved by the expression of {alpha}-enolase and MBP-1. In addition, both {alpha}-enolase and MBP-1 suppressed the N1IC-enhanced colony-forming ability through c-myc. These results indicate that the activated Notch1 receptor and {alpha}-enolase or MBP-1 cooperate in controlling c-myc expression through binding the YY1 response element of the c-myc promoter to regulate tumorigenesis.

* Corresponding author. Mailing address: Department of Anatomy and Cell Biology, School of Medicine, National Yang-Ming University, 155, Sec. 2, Li-Nong St., Taipei 112, Taiwan. Phone: 886-2-2826-7070. Fax: 886-2-2821-2884. E-mail: tsyeh{at}ym.edu.tw

{triangledown} Published ahead of print on 19 May 2008.

Molecular and Cellular Biology, August 2008, p. 4829-4842, Vol. 28, No. 15
0270-7306/08/$08.00+0     doi:10.1128/MCB.00175-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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