Fig. 2
Anti-tumor ability of CUDC-907 in ESCC cell lines. a ESCC Cells were treated with various small molecule inhibitors (30 nM CUDC-907, trichostatin A, pictilisib, respectively), a common chemotherapy agent (3 μM carboplatin), and their combinations or DMSO (0 nM) in a time-dependent manner (0, 24, 48,72 h). Cell viability was confirmed using the CCK-8 experiment. b IC50 of different ESCC cells was calculated using GraphPad Prism. c Apoptosis rates were determined by Annexin V/PI assay after ESCC cells (KYSE-450 and KYSE-510) were exposed to CUDC-907 (5–50 nM) for 24 h. d Cell cycle profile analyses in ESCC cells (KYSE-450 and KYSE-510) exposed to CUDC-907 (10 and 30 nM) for 24 h. e Invasion assays were performed with ESCC cells after being exposed to CUDC-907 (10 and 30 nM) for 24 h by Transwell chambers. Scale bar: 100 μm. f Migration abilities were tested by a wound-healing assay in ESCC cells (KYSE-450 and KYSE-510) exposed to CUDC-907 (10 and 30 nM) for 24 h. Scale bar: 100 μm. g statistical analysis of migration assay and invasion assay. h Immunofluorescence analysis of γ-H2AX foci was performed in ESCC cells (KYSE-450 and KYSE-510) exposed to CUDC-907 (10 and 30 nM) for 24 h. Nuclei were visualized by using DAPI. Scale bar: 20 μm. i Levels of proteins related to the process of apoptosis, cell cycle, DNA damage, and epithelial–mesenchymal-transition (EMT) were measured via western blot analysis after ESCC cells (KYSE-450 and KYSE-510) were exposed to CUDC-907 (10 and 30 nM) for 24 h. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as the loading control. Error bars are ± SD. *P < 0.05; **P < 0.01; ***P < 0.001