Background In a previous study,we have verified that CXCR4 expression is correlated with tumor aggressiveprogression and poor prognosis in patients with epithelial ovarian cancer.The aim of this study was to explore the effectof CXCL12-CXCR4 axis on the metastasis of human ovarian cancer.Methods The expressions of CXCR4 and CXCL12 mRNA and protein in human ovarian cancer cell line CAOV-3 wasdetected by RT-PCR and immunocytochemistry.Methythiazolyltetrazolium(MTT)was used to analyze the effect ofdifferent concentrations of CXCL12 on the proliferation of CAOV-3 cells.Transwell invasion chamber and matrigel wereused to evaluate the effect of various concentrations of CXCL12 and ascites on the migration and invasion of CAOV-3cells.The expressions of integrin β_1 and vascular endothelial growth factor-C(VEGF-C)mRNA were detected byRT-PCR.Data were analyzed using ANOVA by SAS 6.12.Results Under serum-free suboptimal culture conditions,CXCL12(100 ng/ml)significantly enhanced the proliferationof CAOV-3 cells compared with the control and 10 ng/ml CXCL12 groups(0.428±0.051 vs.0.325±0.045 and0.328±0.039,P<0.05).This enhancing effect of CXCL12 was significantly inhibited by 10 μg/ml neutralizing CXCR4antibody or 1 μg/ml CXCR4 antagonist AMD3100.However,10 μg/ml neutralizing CXCR4 antibody could not inhibit cellproliferation without CXCL12.The levels of migration and invasion of the CAOV-3 cells treated with 100 ng/ml CXCL12were significantly higher than those in the control(migration:523.3±25.2 vs 108.0±7.2;invasion:39.3±4.0 vs.4.0±1.0).The enhancing effect of CXCL12 on cell migration and invasion increased with the concentration of CXCL12(100ng/ml vsl0 ng/ml:migration,523.3±25.2 vs 211.7±24.7;invasion,39.3±4.0 vs 15.7±3.1,P<0.05),and was stronglyinhibited by 10 μg/ml neutralizing CXCR4 antibody or 1 μg/ml AMD3100.The number of migrated and invading cells inthe CAOV-3 added with ascites was significantly higher than those in the 100 ng/ml CXCL12 group(migration:706.6±30.6 vs 523.3±25.2,invasion:61.7±7.6 vs 39.3±4.0,P<0.05).The level of integrin β_1 mRNA was greatly increased at3 hours after being treated with CXCL12(0.53±0.10 vs.1.53±0.16,P<0.05),and VEGF-C mRNA displayed significantaugment at 24 hours after being treated with CXCL12(0.52±0.09 vs 1.11±0.15,P<0.05).Conclusions CXCL12 and its receptor CXCR4 can promote the proliferation,migration,invasion of ovarian cancer cellline CAOV-3 and enhance its secretion of integrin β_1 and VEGF-C.These effects can be inhibited by neutralizing CXCR4antibody or AMD3100.CXCL12-CXCR4 axis plays an important role in ovarian cancer growth and metastasis. Background In a previous study, we have verified that CXCR4 expression is correlated with tumor aggressiveprogression and poor prognosis in patients with epithelial ovarian cancer. The aim of this study was to explore the effectof CXCL12-CXCR4 axis on the metastasis of human ovarian cancer. Methods The expressions of CXCR4 and CXCL12 mRNA and protein in human ovarian cancer cell line CAOV-3 wasdetected by RT-PCR and immunocytochemistry. Methythiazolyltetrazolium (MTT) was used to analyze the effect of different concentrations of CXCL12 on the proliferation of CAOV-3 cells. Transwell invasion chamber and matrigel were used to evaluate the effect of various concentrations of CXCL12 and ascites on the migration and invasion of CAOV-3 cells. The expressions of integrin β_1 and vascular endothelial growth factor-C (VEGF-C) mRNA were detected by RT-PCR. Data were analyzed using ANOVA by SAS 6.12. Results Under serum-free suboptimal culture conditions, CXCL12 (100 ng / ml) significantly enhanced the proliferatio nof CAOV-3 cells were compared with the control and 10 ng / ml CXCL12 groups (0.428 ± 0.051 vs. 0.025 ± 0.045 and 0.328 ± 0.039, P <0.05). This enhancing effect of CXCL12 was significantly inhibited by 10 μg / ml neutralizing CXCR4 antibody or 1 μg / ml CXCR4 antagonist AMD3100. However, 10 μg / ml neutralizing CXCR4 antibody could not inhibit cell proliferation without CXCL12. These levels of migration and invasion of the CAOV-3 cells treated with 100 ng / ml CXCL12were significantly higher than those in the control effect of CXCL12 on cell migration and invasion increased with concentration of CXCL12 (100 ng / ml vs 10 ng / ml: migration, 523.3 ± 25.2 vs 211.7 ± 24.7; invasion, 39.3 ± 4.0 vs 15.7 ± 3.1, P <0.05) and was strongly inhibited by 10 μg / ml neutralizing CXCR4 antibody or 1 μg / ml AMD3100.The number of migrated and invading cells inthe CAOV-3 added with ascites was significantly higher than those in the 100 ng / ml CXCL12 group (migratio n: 706.6 ± 30.6 vs523.3 ± 25.2, invasion: 61.7 ± 7.6 vs. 39.3 ± 4.0, P <0.05). The level of integrin β_1 mRNA was greatly increased at3 hours after being treated with CXCL12 (0.53 ± 0.10 vs.1.53 ± 0.16, P <0.05) and VEGF-C mRNA displayed significantaugment at 24 hours after being treated with CXCL12 (0.52 ± 0.09 vs 1.11 ± 0.15, P <0.05) .Conclusions CXCL12 and its receptor CXCR4 can promote the proliferation, migration, invasion of ovarian cancer cellline CAOV-3 and enhance its secretion of integrin β_1 and VEGF-C. These effects can be inhibited by neutralizing CXCR4 antibody or AMD3100.CXCL12-CXCR4 axis plays an important role in ovarian cancer growth and metastasis.