Fig. 6From: Involvement of CXCL12/CXCR4 in the motility of human first-trimester endometrial epithelial cells through an autocrine mechanism by activating PI3K/AKT signalingEEC-derived CXCL12 increased EEC invasion by binding to CXCR4 a Exogenous CXCL12 significantly increased EEC invasion in vitro, whereas neutralizing antibody against CXCR4 or CXCL12 effectively inhibited the CXCL12-stimulated invasion of EECs. b EEC-CM significantly increased EEC invasion in vitro, and a neutralizing antibody against CXCR4 or CXCL12 effectively inhibited EEC-CM-induced invasion of EECs. c CXCR4 or CXCL12 blocking antibody alone markedly inhibited the invasion of EECs. * P < 0.05, ** P < 0.01, compared to the control; # P < 0.05, ## P < 0.01, compared to the CXCL12-treated or EEC-CM-treated group. Data are presented as mean ± SD. (n = 3). EEC: human first-trimester endometrial epithelial cell, EEC-CM: EEC conditioned culture mediumBack to article page