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

Teeranai ITTIUDOMRAK; Songchan PUTHONG; Tanapat PALAGA; Sittiruk ROYTRAKUL; Chanpen CHANCHAO

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

Author: Teeranai ITTIUDOMRAK ¹ ; Songchan PUTHONG ² ; Tanapat PALAGA ³ ; Sittiruk ROYTRAKUL ⁴ ; Chanpen CHANCHAO ⁵
Author Information

1. Program in Biotechnology, Faculty of Science, Chulalongkorn University
2. Institute of Biotechnology and Genetic Engineering, Chulalongkorn University
3. Department of Microbiology, Faculty of Science, Chulalongkorn University
4. National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency
5. Department of Biology, Faculty of Science, Chulalongkorn University
Publication Type:Journal Article
Keywords: Apigenin; Breast cancer; Cell cycle arrest; Necrosis; α-Mangostin
From:Asian Pacific Journal of Tropical Biomedicine 2018;8(11):519-526
CountryChina
Language:Chinese
Abstract: 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 G