Skip to main content
Fig. 4 | BMC Cancer

Fig. 4

From: Arsenic treatment increase Aurora-A overexpression through E2F1 activation in bladder cells

Fig. 4

E2F1 was responsible of arsenic exposure induced Aurora-A overexpression in E7 cells. a E7 cells were co-transfected with pGL2-AAP plasmid (Aurora-A luciferase promoter reporter) and pRLTK (Renilla as an internal control), and treated with arsenic (0, 0.5, 2 and 5 μM) for 24 and 48 h. Data are shown in triplicate as mean ± S.D. of 9 samples from 3 independent experiments. Student’s t test was used *p < 0.05, **p < 0.01 (compared to the value of untreated group). b E7 cells were treated with arsenic (0, 0.5 and 2 μM) for 24 h and total protein was extracted to evaluate E2F1 protein expression with anti-E2F1 antibodies by Western blotting. The same blot was re-probed with antibody against β-actin as the internal control. c Cells were co-transfected with pGL2-AAP plasmid (Aurora-A luciferase promoter reporter), pRLTK (Renilla as an internal control) and different amount of pCMV-E2F1 plasmid which containing full length E2F1 cDNA for 24 and 48 h. The luciferase activity of the cells was evaluated by Dual-Luciferase analysis system. Student’s t test was used as compared to the value of E2F1 untreated one. *p < 0.05, **p < 0.01, ***, p < 0.001. d The enzymatic-sheared chromatin was pulled down with an anti-E2F1 antibody. The two putative E2F1 binding sites (from −268 to −80 and −104 to +106) within Aurora-A promoter was carried out by PCR. e E7 cells were infected with or without lentivirus expressing E2F1 shRNA. After puromycin selection, E2F1 silencing stable cells were treated with 2 μM of arsenic for 2 to 4 days and the protein levels of E2F1 and Aurora-A were evaluated. Quantitative presentation of relative Aurora-A induction by arsenic with E2F1 silencing (sh E2F1) or without E2F1 silencing (wild type E2F1). P < 0.05 (compared to the cells without arsenic treatment). The data were analyzed by Student’s t test

Back to article page