EG-1 interacts with c-Src and activates its signaling pathway.
EG-1 is significantly elevated in breast, colorectal, and prostate cancers. Overexpression of EG-1 stimulates cellular proliferation, and targeted inhibition blocks mouse xenograft tumor growth. To further clarify the function of EG-1, we investigated its role in c-Src activation. We observed that EG-1 overexpression results in activation of c-Src, but found no evidence that EG-1 is a direct Src substrate. EG-1 also binds to other members of the Src family. Furthermore, EG-1 shows interaction with multiple other SH3- and WW-containing molecules involved in various signaling pathways. These observations suggest that EG-1 may be involved in signaling pathways including c-Src activation.
Lu
Ming
M
Department of Surgery, Division of Oncology, UCLA School of Medicine, Los Angeles, CA, USA.
Zhang
Liping
L
Sartippour
Maryam R
MR
Norris
Andrew J
AJ
Brooks
Mai N
MN
D045744:Cell Line, Tumor; D004789:Enzyme Activation; D006801:Humans; D056892:Mediator Complex; D009369:Neoplasms / Q000201:enzymology*; D025941:Protein Interaction Mapping; D017434:Protein Structure, Tertiary; D011506:Proteins / Q000378:metabolism*; D016392:Proto-Oncogene Proteins pp60(c-src) / Q000378:metabolism*; D015398:Signal Transduction; D015533:Transcriptional Activation; D018909:src Homology Domains
C496877:MED28 protein, human; D056892:Mediator Complex; D011506:Proteins; D016392:Proto-Oncogene Proteins pp60(c-src)