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BASIC RESEARCH
Year : 2018  |  Volume : 8  |  Issue : 11  |  Page : 519-526

α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation


1 Program in Biotechnology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok 10330, Thailand
2 Institute of Biotechnology and Genetic Engineering, Chulalongkorn University, 254 Phayathai Road, Bangkok 10330, Thailand
3 Department of Microbiology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok 10330, Thailand
4 National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency, Pathum Thani, Thailand
5 Department of Biology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok 10330, Thailand

Correspondence Address:
Chanpen Chanchao
Department of Biology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok 10330
Thailand
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2221-1691.245956

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Objective: To find new compounds in order to overcome the mainstay of metastatic breast cancer due to the adverse side effects from, and increasing resistance to, current chemotherapeutic agents. Methods: α-Mangostin and apigenin were reported in comparison to doxorubicin, a chemotherapeutic drug. Ductal carcinoma (BT474) cell line and non-tumorigenic epithelial tissue from mammary gland (MCF-10A) were used. Cell viability assessment was calculated by the standard 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. Cell morphology was investigated by light microscopy. By flow cytometry analysis, programmed cell death was observed using annexin V and propidium iodide staining while cell-cycle arrest was observed using propidium iodide staining. Change in transcriptional expression was evaluated by real-time quantitative reverse transcription PCR. Results: In 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, the result revealed α-mangostin and apigenin were more cytotoxic to BT474 cells. Longer exposure times to α-mangostin and apigenin caused more floating cells and a lower density of adhered cells with more vacuoles present in the colonies in BT474 only. α-Mangostin and apigenin caused necrosis in BT474 cells in a 24 h exposure, but a small amount of early apoptotic cells could also be detected at 24, 48 and 72 h exposure, whereas doxorubicin caused early apoptosis to BT474 cells at 24 h. Transcript expression and activity analysis supported caspase-3 was involved in the death of BT474 cells treated by all compounds. Moreover, α-mangostin and apigenin arrested the cell-cycle at the G1-phase, but at the G2/M-phase by doxorubicin. All three compounds induced a change in transcript expression levels of inflammation-associated, proto-oncogene, autophagy-associated and apoptosis-associated genes. Conclusions: α-Mangostin and apigenin are worth investigating as potential new sources of chemotherapeutic agents for breast cancer treatment.


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