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J. Biol. Chem., Vol. 279, Issue 19, 19407-19420, May 7, 2004

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Unique and Selective Effects of Five Ets Family Members, Elf3, Ets1, Ets2, PEA3, and PU.1, on the Promoter of the Type II Transforming Growth Factor- Receptor Gene^*

Janel L. Kopp¶, Phillip J. Wilder¶, Michelle Desler, Jae-Hwan Kim||, Jingwen Hou, Tamara Nowling**, and Angie Rizzino

From the Eppley Institute for Research in Cancer and Allied Diseases and the Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-6805

Previous studies have shown that the promoter of the type II TGF- receptor gene (TR-II) is strongly stimulated by Elf3, a member of the Ets transcription factor family. The TR-II gene behaves as a tumor suppressor and it is expressed in nearly all cell types, whereas Elf3 is expressed primarily in epithelial cells. Hence, the TR-II gene is likely to be regulated by other Ets proteins in nonepithelial cells. In this study, we examined the effects of four other Ets family members (Ets1, Ets2, PEA3, and PU.1) on TR-II promoter/reporter constructs that contain the two essential ets sites of this gene. These studies employed F9 embryonal carcinoma cells and their differentiated cells, because transcription of the TR-II gene increases after F9 cells differentiate. Here we demonstrate that Ets2, which is expressed in F9-differentiated cells along with Elf3, does not stimulate or bind to the TR-II promoter in these cells. In contrast, PEA3 stimulates the TR-II promoter in F9-differentiated cells, but it inhibits this promoter in F9 cells. Thus, the effects of PEA3 on the TR-II promoter are cell context-dependent. We also show that the effects of Elf3 are cell context-dependent. Elf3 strongly stimulates the TR-II promoter in F9-differentiated cells, but not in F9 cells. In contrast to Elf3 and PEA3, Ets1 strongly stimulates this promoter in both F9 cells and F9-differentiated cells. Finally, we show that PU.1 exerts little or no effect on the activity of the TR-II promoter. Together, our findings indicate that Elf3 is not the only Ets protein capable of stimulating the TR-II promoter. Importantly, our findings also indicate that each of the five Ets proteins influences the TR-II promoter in a unique manner because of important differences in their biochemical properties or their patterns of cellular expression.

Received for publication, December 23, 2003 , and in revised form, February 12, 2004.

^* This work was supported by National Cancer Institute Grant CA 74771 and Nebraska Department of Health Grant 9127. Core facilities of the University of Nebraska Medical Center Eppley Cancer Center were supported in part by Cancer Center Support Grant CA36727. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ These authors contributed equally to this manuscript.

^|| Current address: Cell and Gene Therapy Research Inst., Pochon CHA University, 135-081 Seoul, South Korea.

^** Current address: Dept. of Medicine; Medical University of South Carolina, Charleston, SC 29425.

To whom correspondence should be addressed: Eppley Inst. for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, NE 68198-6805. Tel.: 402-559-6338; Fax: 402-559-4651; E-mail: arizzino{at}unmc.edu.

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