Fig. 3: EphA2 mediates proliferation, migration, invasion, and sorafenib sensitivity. | Experimental & Molecular Medicine

Fig. 3: EphA2 mediates proliferation, migration, invasion, and sorafenib sensitivity.

From: Quantitative phosphoproteomic analysis identifies the potential therapeutic target EphA2 for overcoming sorafenib resistance in hepatocellular carcinoma cells

Fig. 3

a HuH-7R cells were infected with lentiviruses containing shEphA2 (#1, #2) or control shRNA (shCtrl) and, 48 h later, were lysed and analyzed by western blotting with the indicated antibodies. b The viability of EphA2 knockdown HuH-7R cells was determined at the indicated time points with the MTT assay. The plots depict cumulative cell numbers versus days in culture. c The tumorigenicity of EphA2 knockdown HuH-7R cells was determined using the soft agar colony-formation assay. d Wound-healing assay of shEphA2-infected HuH-7R cells. The micrographs show cells that migrated into the gap 0 and 24 h after the removal of the insert. e Transwell invasion assay of shEphA2-infected HuH-7R cells. Cells in the central field of each insert were visualized via light microscopy and quantified. f HuH-7, shCtrl, and shEphA2-containing HuH-7R cells were exposed to sorafenib at the indicated concentrations for 72 h, and cell viability was analyzed with the MTT assay. The concentration–response curve for sorafenib in the EphA2 knockdown group shifted toward a lower concentration compared to that for shCtrl-infected HuH-7R cells. All statistical data were calculated from three independent replicates (**p < 0.01; ***p < 0.001; shCtrl control shRNA, shEphA2 shRNA against EphA2).

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