Endothelial Genes
Abstract
We report that EG-l can stimulate cellular proliferation. Transfection experiments which overexpressed the full length EG-l gene in human embryonic kidney HEK-293 cells or human breast cancer cell lines resulted in significantly increased in vitro proliferation, in comparison to transfection with empty vectors. On the other hand, siRNA co-transfection resulted in inhibition of proliferation. A subcutaneous xenograft assay was carried out in a SCID (severe combined immunodeficient) mouse model. We found that injection of high EG-l expressing llEK-293 clones resulted in significantly larger tumors, in comparison with clones carrying the enipty vectors. To fi%ther clari?y the function of this gene, we investigated its interaction with Src and members of the MAPK (mitogen activated protein kinase) family. Immunoprecipitation with anti-Src antibody, followed by immunoblotting with anti-EG- 1 antibody demonstrated an association between these two molecules. Over- expression %fEG-l was correlajed with activation of the following kinases: ERK-l and -2 (extracellular signal- regulated), JNK Uun-terminal), and p38. These observations collectively support the hypothesis that the novel gene EG-I is a positive stimulator of cellular proliferation, and may possibly be involved in signaling pathways involving Src and MAPK activation.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2005
- Accession Number
- ADA439227
Entities
People
- Mai H. Nguyen Brooks
Organizations
- University of California, Los Angeles