Figures & data
Figure 1. The cell viability of HCPT and CRI alone or in combination in H460 (A), H1975 (B), and HCC827 (C) cells as well as the toxicity to BEAS-2B and HUVEC cells (D). Cell viability was assessed by MTT assay. Cancer cells were treated with various concentrations (0, 0.001, 0.01, 0.1, 1, and 10 μM) of HCPT and CRI alone for 48 h (H460 cells) or 72 h (H1975 and HCC827 cells) (upper panel). For the middle panel, the lung cancer cells were treated with the combination of HCPT and CRI. CI values for the combination were calculated by the CompuSyn software (lower panel). HCPT (0.125 μM) combined with CRI (1, 2, 4, 8 μM) showed a synergistic effect on H460 cells. The combination of HCPT and CRI (0.5–12 μM) exhibited a synergistic effect on H1975 and HCC827 cells at the ratio of 1:10 and 1:4. IC50 was calculated by GraphPad software.
Figure 2. The morphological features of cancer cells and effect on cancer cells proliferation after HCPT and CRI alone or in combination treatment. The fluorescence intensity and colony formation of H460 (A), H1975 (B), and HCC827 (C) cells were significantly decreased when treated with HCPT and CRI. *p < 0.05, vs control group.
Figure 4. The regulation of HCPT and CRI on EGFR downstream signalling pathways in H460 (A), H1975 (B), and HCC827 (C) cells. The total proteins and phosphorylated proteins related to EGFR signalling pathway including AKT, JNK, ERK, and p38 MAPK were detected after treated with HCPT and CRI alone or in combination.
Figure 5. The in vitro effect of compounds CH-1 and CH-2 on lung cancer cells and normal cells. The cytotoxicity of compounds CH-1 and CH-2 on H460 (A), H1975 (B), and HCC827 (C) cells was dose-dependent. The compounds CH-1 and CH-2 had little toxicity to BEAS-2B and HUVEC cells (D and E).
Scheme 1. Synthesis of compound CH-1.
Scheme 2. Synthesis of compound CH-2.
