Resveratrol, a naturally occurring stilbene, induced apoptosis in human breast cancer MCF-7 cells. The mechanism of this effect was dependent on mitogen-activated protein kinase (MAPK, ERK1/2) activation and was associated with serine phosphorylation and acetylation of p53. Treatment of MCF-7 cells with resveratrol in the presence of 17β-oestradiol (E2) further enhanced MAPK activation, but E2 blocked resveratrol-induced apoptosis, as measured by nucleosome ELISA and DNA fragmentation assays. E2 inhibited resveratrol-stimulated phosphorylation of serines 15, 20 and 392 of p53 and acetylation of p53 in a concentration- and time-dependent manner. These effects of E2 on resveratrol action were blocked by ICI 182,780 (ICI), an inhibitor of the nuclear oestrogen receptor-α (ER). ICI 182,780 did not block the actions of resveratrol, alone. Electrophoretic mobility studies of p53 binding to DNA and of p21 expression indicated that E2 inhibited resveratrol-induced, p53-directed transcriptional activity. These results suggest that E2 inhibits p53-dependent apoptosis in MCF-7 cells by interfering with post-translational modifications of p53 which are essential for p53-dependent DNA binding and consequent stimulation of apoptotic pathways. These studies provide insight into the complex pathways by which apoptosis is induced by resveratrol in E2-depleted and -repleted environments.

Objectives: To study the effect of Tspan5 on the proliferation and migration of trophoblast cells. Materials and Methods: The authors silenced the Tspan5 expression in human choriocarcinoma cell line JEG-3 using RNAi, and then conducted the cell proliferation assay and scratch assay to detect the proliferation and migration of JEG-3 cells. Results: The present authors found that the JEG-3 cell proliferation and migration activity of interference group (Tspan5/1005) had decreased significantly. Tspan5/1005 moderately decreased FAK and AKT phosphorylation compared to the control group. In this study, the authors found that the proliferation and migration of choriocarcinoma cells were reduced after using RNAi technology to downregulate the expression level of Tspan5 expression. The level of Tspan5 expression was positively correlated with the proliferation and migration of choriocarcinoma cells. Conclusions: Tspan5 could play a biological role through the FAK/AKT signaling pathway.