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. 2020 Mar 31;12(4):841. doi: 10.3390/cancers12040841

Figure 4.

Figure 4

DDR1 kinase inhibitors suppressed OSCC cell growth and clonogenicity. Drug sensitivity (left part in each panel) was determined by treating cells with 2–10 μM imatinib. (a) 0.01–1 μM dasatinib, (b) or 0.024–15 μM DDR1-IN-1 (c) for 3 d, followed by WST-1 proliferation assay. VC, vehicle control (H2O for imatinib; DMSO for dasatinib and DDR1-IN-1). For each treatment, data are presented as mean ± SD from quadruplicate wells. Breast cancer cell line T-47D served as a control. Similar results were obtained from two independent experiments; one set of data is shown. Clonogenic survival assay (right part in each panel) was determined by treating cells in quadruplicate wells with 10 μM imatinib, (a) 1 μM dasatinib (b) or 10 μM DDR1-IN-1 (c) for 24 h, followed by cultivating cells in drug-free media for an additional 10–14 d. Representative photographs of crystal violet staining for each treatment are shown. Colony counts from two independent experiments are presented as mean ± SD, with the VC group set to 100%. * p < 0.05.