Environmental estrogen bisphenol AF enhanced proliferation and invasion of neuroblastoma SH-SY5Y cell line in vitro

Objective To declare the activity of environmental estrogen bisphenol AF (BPAF) in neuroblastoma proliferation or invasion and the effect of BPAF on the transcriptional activity of estrogen receptor α(ERα). Methods SH-SY5Y cells, which were transfected with ERE-Luc or CatD-Luc, were treated with indicated dose (0.01μmol/L, 0.03μmol/L, 0.1μmol/L, 0.3μmol/L, 1μmol/L, 3μmol/ L and 10μmol/L) of BPAF. Next, cells were harvested and analyzed by luciferase assays. Then, SH-SY-5Y cells were seeded in 96-well plates and were treated by EC_maxof BPAF. The growth curves for each cell group were drawn according to the volume of O.D. 450 nm. The siRNA (small interfere RNA) of ERα or its antagonist (ICI-182780) was used to declare the specificity of BPAF function, and ERα expression vector was transfected by MDA-MB-231 cells in triple negative breast cancer (TNBC). SH-SY5Y cells were treated with EC_maxof BPAF after transfection with ERα siRNA or treatment with ICI-182780 (100 nmol/L). Then, the induction of BPAF to ERα transcriptional activity and its promoted effect on proliferation and invasion of SH-SY5Y cells was detected. Results Treatment of BPAF induced the transcriptional activity of ERα in a dose dependent manner EC₅₀=(0.44±0.09)μmol/L, R²=0.94, P=0.007 6, and the EC_maxvalue of BPAF on ERα activity was 3μmol/L. Transfection of ERα siRNA could disrupt the activity of ERα induced by BPAF (3μmol/L) significantly (inhibition rate, IR=76.97%), SH-SY5Y proliferation (IR=77.42%) and invasion (IR=95.87%). Treatment of 100 nmol/L ICI-182780 also inhibited ERα activity (IR=77.75%), SH-SY5Y proliferation (IR=86.76%) and invasion (IR=105.56%). Conclusion BPAF will promote the proliferation or invasion of neuroblastoma cells by inducing the transcription factor activity of ERα.