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Fig. 2 | BMC Cancer

Fig. 2

From: Epoxyazadiradione suppresses breast tumor growth through mitochondrial depolarization and caspase-dependent apoptosis by targeting PI3K/Akt pathway

Fig. 2

Epoxyazadiradione inhibits cell viability in TNBC and ER+ breast cancer cells through induction of apoptosis: a and b MDA-MB-231 (1 × 104) and MCF-7 (1 × 104) cells were seeded into 96-well plate and treated with increasing concentrations of epoxyazadiradione (0–200 μM) for 24 h. Cell death induced by epoxyazadiradione was analyzed by MTT assay. The percentage inhibition of cell viability represented graphically. c MDA-MB-231 cells were treated with epoxyazadiradione at indicated doses for 24 h and cells were stained with annexin V-FITC and propidium iodide and analyzed by flow cytometer. The percentage of apoptotic cells were quantified and represented into bar graph from three independent experiments. d Chromatin condensation or nuclear fragmentations were analysed by DAPI staining or TUNEL assay using fluorescence microscope in MDA-MB-231 cells in presence of epoxyazadiradione at indicated concentrations. Arrows indicate the chromatin condensation and nuclear fragmentation. The actin disorganization was examined in epoxyazadiradione treated MDA-MB-231 cells using phalloidin FITC staining and analyzed by confocal microscopy. Values are represented in mean ± SEM of three independent experiments in each case or representative of a typical experiment: *, p < 0.02; **, p < 0.006; ***, p < 0.0004 by one-way ANOVA

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