Fig. 6From: Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cellsThe effects of PA on ER stress, autophagy, cell viability as well as apoptosis. a The relative expression levels of CHOP, BIP, ATF6, IRE1 and PERK in cells treated with/without 4 μm α-mangostin followed 24 h incubation with/without 10 μM PA were analyzed by western blot and quantified. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01. b The relative expression levels of LC3II/LC3I and P62 in cells treated with/without 4 μm α-mangostin followed 24 h incubation with/without 10 μM PA were analyzed by western blot and quantified. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01. c Cells were treated with/without 4 μm α-mangostin followed 24 h incubation with/without 10 μM PA. Cell viabilities were then determined by the CCK-8 assay. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01. d The percentage of apoptotic cells in each well was counted under flow cytometry. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01. e Cells were treated with/without 4 μm α-mangostin followed 24 h incubation with/without 10 μM PA and double-stained with annexin V and PI and analyzed by flow cytometry. The gate setting distinguished between living (bottom left), necrotic (top left), early apoptotic (bottom right), and late apoptotic (top right) cellsBack to article page