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. 2019 Apr 26;10:867. doi: 10.3389/fimmu.2019.00867

Figure 4.

Figure 4

Atezolizumab in combination with Bevacizumab inhibit proliferation, migration, and invasion of cisplatin resistant ovarian cancer cell line A2780cis synergistically, which may be related to Bevacizumab suppresses the epithelial-mesenchymal transition (EMT) and PD-L1 expression by targeting STAT3. (A) Cell apoptosis rate of A2780cis was significantly lower than A2780 (*P < 0.05), which proved A2780cis was the cisplatin-resistant cell line. (B) Based the different concentrations (0.01, 0.1, 1.0, 5.0, and 10.0μg/mL) of Bevacizumab to treat A2780cis, the proliferation of cells was obviously inhibited by using of 5.0 μg/mL Bevacizumab (*P < 0.05). (C) Based the different concentrations (0.1, 1.0, 5.0, 10.0, and 20.0 μg/mL) of Atezolizumab to treat A2780cis, the proliferation of cells was obviously inhibited by using of 10.0 μg/mL Atezolizumab (*P < 0.05). (D) The inhibition rate of A2780cis cell proliferation was dramatically increased after treated by Bevacizumab (5.0 μg/mL) and Atezolizumab (10.0 μg/mL) using CCK-8 assay (*P < 0.05). The wound healing assays (E) and transwell assay (F) showed that Bevacizumab and Atezolizumab impaired A2780cis cell migration and invasion, respectively (*P < 0.05). (G) Mesenchymal marker proteins (vimentin and β-catenin) and EMT-mediating transcription factor (Snail and Slug) were down-regulated in A2780cis cells after treated by Bevacizumab or/and Atezolizumab, while the epithelial marker E-cadherin was up-regulated, especially under the combination of them. (H) The activation of STAT3 and expression of PD-L1 in A2780cis cells were decreased by Bevacizumab treatment. Thus, these findings strongly suggested that Bevacizumab inhibit EMT and PD-L1expression via down-regulating the phosphorylation of STAT3.