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  • Title: Anticancer effects of α-mangostin in OVACAR-3 human ovarian carcinoma cells are mediated via involvement of reactive oxygen species, mitochondrial -mediated apoptosis, suppression of cell migration and invasion and m-TOR/PI3K/AKT signaling pathway.
    Author: Yu Y, Fei Z, Qin L.
    Journal: J BUON; 2020; 25(5):2293-2300. PubMed ID: 33277848.
    Abstract:
    PURPOSE: α-mangostin belongs to xanthone class of natural products, showing a great biological and pharmacological potential. α-mangostin has shown remarkable anticancer potential against different cancer cell lines. Herein, α-mangostin was tested for its anticancer potential against human ovarian cancer cell line (OVACAR-3). Its effects on reactive oxygen species (ROS), mitochondrial-mediated apoptosis, cell migration and invasion and m-TOR/PI3K/AKT signaling pathway, was also determined. METHODS: MTT assay was performed to evaluate the rate of proliferation and clonogenic assay was used to assess the effects of α-mangostin on OVACAR-3 cell colonies. Phase contrast microscopy was implemented to evaluate cellular morphology. Acridine orange (AO) and ethidium bromine (EB) staining was used to check apoptosis along with western blotting. JC-1 and DCFH-DA staining assays were performed for the determination of mitochondrial membrane potential (MMP) and ROS, respectively. Cell migration and invasion analysis was performed with transwell chambers assay. The effect on m-TOR/PI3K/AKT signaling pathway was monitored by western blotting assay. RESULTS: α-mangostin had a tremendous inhibitory effect on cell proliferation rate in OVACAR-3 cells in a dose-dependent manner. The number of colonies was also observed to decline in a dose-dependent manner. Phase contrast microscopy showed significant morphological changes in OVACAR-3 cells after α-mangostin exposure. The antiproliferative effects were due to mitochondrial-mediated apoptosis. MMP was decreased by α-mangostin exposure and ROS production enhanced dose-dependently. Cell migration and invasion were also decreased by α-mangostin in OVACAR-3 cells. Finally, α-mangostin was observed to block the m-TOR/PI3K/AKT signaling pathway in OVACAR-3 cells. CONCLUSION: α-Mangostin could induce antiproliferative effects against OVACAR-3 cells mediated via ROS production, mitochondrial-mediated apoptosis and inhibition of m-TOR/PI3K/AKT signalling. Therefore, it may prove a lead molecule in ovarian cancer treatment.
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