!Name=RERG_Breast !ExptSetNo=1443 !Description=Using microarray analysis, we identified a unique ras superfamily gene, termed RERG (ras-related and estrogen-regulated growth inhibitor), whose expression was decreased or lost in a significant percentage of primary human breast tumors that show a poor clinical prognosis. Importantly, high RERG expression correlated with expression of a set of genes that define a breast tumor subtype that is estrogen receptor-positive and associated with a slow rate of tumor cell proliferation and a favorable prognosis for these cancer patients. RERG mRNA expression was induced rapidly in MCF-7 cells stimulated by beta-estradiol and repressed by tamoxifen treatment. Like Ras, RERG protein exhibited intrinsic GDP/GTP binding and GTP hydrolysis activity. Unlike Ras proteins, RERG lacks a known recognition signal for COOH-terminal prenylation and was localized primarily in the cytoplasm. Expression of RERG protein in MCF-7 breast carcinoma cells resulted in a significant inhibition of both anchorage-dependent and anchorage-independent growth in vitro and inhibited tumor formation in nude mice. These features of RERG are strikingly different from most Ras superfamily GTP-binding pro-teins and suggest that the loss of RERG expression may contribute to breast tumorigenesis. !Name=MCF7-UCLA estrogen starved 2days X MCF7+E2 24hrs !Exptid=11773 !Name=MCF7-UCLA estrogen starved 2days X MCF7+E2 8hrs !Exptid=11792 !Name=MCF7-UCLA estrogen starved 2days#2 X MCF7+E2 4hrs !Exptid=9476 !Name=MCF7-UCLA X MCF7+1um Tamoxifen 48hrs !Exptid=7823 !Name=MCF7-UCLA X MCF7+6um Tamoxifen 48hrs #1 !Exptid=8996