“…For example, studies in this laboratory and others have demonstrated that deletion and mutational analysis of promoters derived from several E 2 -responsive genes contain GC-rich motifs that bind Sp proteins (Safe & Kim 2004). Some of the genes that fall into this category are important for cell proliferation, angiogenesis, and nucleotide metabolism and include E 2 F1, retinoic acid receptor a (RARa), carbamoylphosphate synthetase/ aspartate transcarbamylase/dihydroorotase (CAD), bcl-2, DNA polymerase a, vascular endothelial growth factor (VEGF), VEGFR receptor 2 (VEGFR2), progesterone receptor, creatine kinase B, thymidylate synthase, insulinlike growth factor binding protein 4, epidermal growth factor receptor, receptor for advanced glycation end products, low density lipoprotein receptor, vitamin D receptor, pS2, LRP16, metastasis associated protein 3, and SK3 (Porter et al 1996, Duan et al 1998, Sun et al 1998, 2005, Qin et al 1999, Xie et al 1999, 2000, Byrne et al 2000, Salvatori et al 2000, Saville et al 2000, Stoner et al 2000, Tanaka et al 2000, Castro-Rivera et al 2001, Li et al 2001, Bruning et al 2003, Jacobson et al 2003, Khan et al 2003, Ngwenya & Safe 2003, Schultz et al 2003, 2005, Fujita et al 2004, Bardin et al 2005, Zhao et al 2005, Higgins et al 2006b). In addition, RNA interference studies with a small inhibitory RNA (siRNA) for Sp1 (iSp1) show that after transfection with iSp1, there was a significant decrease in hormone-induced G 0 /G 1 to S-phase progression, suggesting that ERa/Sp1 plays an important role in this process (Abdelrahim et al 2002).…”