Skip to main content
. 2017 Aug 10;8(59):99482–99494. doi: 10.18632/oncotarget.20107

Figure 2. ZEB1 was involved in the migration, invasion, adhesion to mesothelial cells, and PTX sensitivity of EOC cells.

Figure 2

(A) The expression of ZEB1 in various EOC cells. ZEB1 was highly expressed in ES-2, TOV21G, A2780, and HEY cells. (B) Depletion of ZEB1 in ES-2 and SKOV3 cells and influence on expression of E-cadherin as an epithelial marker, and vimentin and N-cadherin as mesenchymal markers. (C, D) Effect of ZEB1 silencing on the migratory ability (C) and invasive potential (D) of ES-2 and SKOV3 cells. Asterisks show significance (P < 0.05). (E, F) Effect of ZEB1 silencing on the attachment of EOC cells to the confluent monolayer of human peritoneal mesothelial cells (HPMCs) (E) ES2 cells, (F) SKOV3 cells). Asterisks show significance (P < 0.05). (G, H) Restoration of PTX-resistance in ES-2 and SKOV3 cells by ZEB1 silencing. The PTX-sensitivity assay using evaluated by the MTT assay (G). Asterisks show significance (P < 0.05). ZEB1 knockdown clearly increased the sensitivities to PTX. IC50 values of PTX were significantly reduced by ZEB1 depletion in ES-2 and SKOV3 cells (H).