This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lu, M. Articles by Brooks, M. N. Search for Related Content PubMed PubMed Citation Articles by Lu, M. Articles by Brooks, M. N.

The Novel Gene EG-1 Stimulates Cellular Proliferation

Department of ¹ Surgery, Division of Oncology, and ² Department of Pathology, School of Medicine, and ³ Department of Chemistry and Biochemistry, University of California at Los Angeles, Los Angeles, California

Requests for reprints: Mai N. Brooks, University of California at Los Angeles, Box 951782, Los Angeles, CA 90095. Phone: 310-206-2215; Fax: 310-825-7575; E-mail: maibrooks{at}mednet.ucla.edu.

We recently discovered a novel gene and named it endothelial-derived gene 1 (EG-1). Previously, we have shown that the expression of EG-1 is significantly elevated in the epithelial cells of breast cancer, colorectal cancer, and prostate cancer. Here, we report that EG-1 can stimulate cellular proliferation. Transfection experiments which overexpressed the full-length EG-1 gene in human embryonic kidney HEK-293 cells or human breast cancer cell lines resulted in significantly increased in vitro proliferation, in comparison with transfection with empty vectors. On the other hand, small interfering RNA cotransfection resulted in inhibition of proliferation. S.c. xenograft assays were carried out in a severe combined immunodeficient mouse model. We found that injection of high EG-1 expressing HEK-293 clones resulted in significantly larger tumors, in comparison with clones carrying the empty vectors. To further clarify the function of this gene, we investigated its interaction with Src and members of the mitogen-activated protein kinase (MAPK) family. Immunoprecipitation with anti-Src antibody, followed by immunoblotting with anti–EG-1 antibody, showed an association between these two molecules. Overexpression of EG-1 was correlated with activation of the following kinases: extracellular signal-regulated kinases 1 and 2, c-jun-NH₂-kinase, and p38. These observations collectively support the hypothesis that the novel gene EG-1 is a positive stimulator of cellular proliferation, and may possibly be involved in signaling pathways involving Src and MAPK activation.

This article has been cited by other articles:

				K. S. Beyer, R. L. Beauchamp, M.-F. Lee, J. F. Gusella, A. M. Naar, and V. Ramesh Mediator Subunit MED28 (Magicin) Is a Repressor of Smooth Muscle Cell Differentiation J. Biol. Chem., November 2, 2007; 282(44): 32152 - 32157. [Abstract] [Full Text] [PDF]