Research Article

Alterations in Cell Cycle and Induction of Apoptotic Cell Death in Breast Cancer Cells Treated with α-Mangostin Extracted from Mangosteen Pericarp

Figure 3

Cytochrome 𝑐 expression, Bid cleavage, and cell-cycle distribution of MDA-MB231 cells after α-mangostin treatment. (a) Cytochrome 𝑐 in mitochondria, as determined by flow cytometry (black line indicates α-mangostin-treated cells and gray line indicates controls). The levels of cytochrome 𝑐 protein in mitochondrial fractions were significantly lower in cells treated with α-mangostin for 24 h (b). Western blots of cytochrome c (15 kDa) showed significant decreases in cells treated with α-mangostin for 24 h, as compared to controls (upper panel). In α-mangostin-treated cells, cytochrome 𝑐 was released from mitochondria, leading to decreases in concentration. β-Actin served as an internal control (lower panel, same in (c)). (c) Western blots of Bid (22 kDa) in control cells and cells treated with α-mangostin for 24 h were similar (upper panel). Cleaved Bid was not observed after α-mangostin treatment. Three samples were used for all analyses in (a)–(c). (d) Cell-cycle analysis confirmed that α-mangostin induced arrest in the G1-phase and inhibition of cells entering the S-phase in MDA-MB231 cells (** 𝑃 < 0 . 0 1 ). Data are presented as mean ± SD of triplicate, independent measurements.
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