We recently discovered a novel gene and named it EG-1. Previously, we have demonstrated that the expression of EG-1 is significantly elevated in breast cancer, colorectal cancer, and prostate cancer. We have also reported that overexpression of EG-1 stimulates cellular proliferation, and that targeted inhibition of this novel gene blocks tumor growth. To further clarify the function of this gene, we investigated EG-1’s interaction with c-Src and members of the MAPK (mitogen activated protein kinase) family. We observed that EG-1 overexpression results in c-Src activation. However, EG-1 is not a direct substrate of c-Src. Also, we found that EG-1 shows protein-protein interaction with the Src family of protein tyrosine kinases (c-Src, Yes, and Fyn). Targeted EG-1 inhibition by specific antibody was correlated with less activation of ERK-1 and -2 (extracellular signal-regulated), p38 and JNK (Jun-terminal) kinases. These observations collectively support the hypothesis that the novel gene EG-1 may be involved in signaling pathways involving c-Src activation and the MAPK family.
[Proc Amer Assoc Cancer Res, Volume 47, 2006]