Figures & data
Figure 1. Chemical structure of AB. AB inhibits cell viability in a concentration-dependent manner on MCF-7/ADR cell line. Values are presented as the mean ± SD of at least three independent experiments. AB: Annosquacin B.
Table 1. The multidrug resistance of MCF-7/ADR cells.
Figure 2. Representative images (200×) of fluorescent microscopic analysis of MCF-7/ADR cells without treatment (control) and treated with 3.5, 7, 14 μM of AB. Cells are stained with AO/EB.
Figure 3. Apoptosis of MCF-7/ADR cells detected by Annexin V-FITC/propidium iodide assay. Cells were treated with or without AB for 48 h, then the cells were stained with Annexin V-FITC and propidium iodide before subjecting to flow cytometry. Lower right part (Annexin V+/PI−) was considered as early apoptotic cells. Higher right part (Annexin V+/PI+) was considered as late apoptosis cells.
Figure 4. Effects of AB on the expression of caspase-3, caspase-9, the ratio of Bax/Bcl-2 on MCF-7/ADR cells. Cells were treated with or without AB for 48 h at indicated concentrations (A). Cells were treated with 14 μM AB in the presence or absence of 10 μM Z-VAD-FMK (B). c-caspase-3: cleaved-caspase-3; c-caspase-9: cleaved-caspase-9; AB: Annosquacin B; Z: Z-VAD-FMK. Values are presented as the means ± SD, n = 3. *p < 0.05, **p < 0.01 versus vehicle control. β-actin was employed as an internal control.
Figure 5. Cell viability was measured by MTT assay, after treatment with 14 μM AB in the presence or absence of 25 μM SB202190 or SP600125 (A). Cells were treated with 14 μM AB in the presence or absence of 10 μM U0126 (B). Effects of p38 MAPKs pathways in AB-induced apoptosis. Cells were treated with 0–14 μM AB for 24 h (C) or 14 μM AB for 0–12 h (D). AB: Annosquacin B; SB: SB202190; SP: SP600125. Values are presented as the means ± SD, n = 3. *(#)p < 0.05, **(##)p < 0.01 versus vehicle control. β-actin was employed as an internal control.
