Endostar blocks the metastasis, invasion and angiogenesis of ovarian cancer cells.

Endostar (ES) inhibits metastasis in some tumors, but its role in ovarian cancer invasion has not been elucidated. In this study, the effects of ES on ovarian cancer cells were further analyzed, to excavate an effective strategy for treating ovarian cancer. Ovarian cancer cell lines (SKOV3 and HO-8910PM) were treated with different concentrations of ES. Cell activity and half-maximal inhibitory concentration (IC50) detected by MTT were used for subsequent experiments. The migration and invasion abilities of treated cells were detected by wound healing and Transwell assays. The expressions of epithelial-mesenchymal transition (EMT)-related proteins in treated cells were determined by western blot analysis. Moreover, in vitro angiogenesis, the expressions of related proteins in treated cells and STAT3, and PD-L1 expressions were determined. We found that with the increase of ES concentrations, the cell activity showed a decreasing trend, and that the compositive IC50 of SKOV3 and HO-8910PM was 50 μg/ml. Moreover, ES observably inhibited migration, invasion, and EMT of ovarian cancer cell lines. In angiogenesis experiments, the angiogenesis ability and the expressions of related proteins in ovarian cancer cell lines were downregulated after ES treatment. Furthermore, ES reduced the expression of PD-L1 and suppressed the phosphorylation of STAT3 in ovarian cancer cell lines. ES blocked the metastasis, invasion, and angiogenesis of ovarian cancer cells by suppressing the activation of PD-L1 and STAT3, which might be considered as the potential mechanism of ES in the treatment of ovarian cancer.