Please use this identifier to cite or link to this item: http://cuir.car.chula.ac.th/handle/123456789/61736
Title: α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation
Authors: Teeranai Ittiudomrak
Songchan Puthong
Tanapat Palaga
Sittiruk Roytrakul
Chanpen Chanchao
Email: No information provided
Songchan.P@Chula.ac.th
Tanapat.P@Chula.ac.th
No information provided
Chanpen.C@Chula.ac.th
Other author: Chulalongkorn University. The Institute of Biotechnology and Genetic Engineering
Chulalongkorn University. Faculty of Science
Subjects: α-Mangostin
Apigenin
Breast cancer
Cell cycle arrest
Necrosis
Issue Date: Nov-2018
Publisher: Wolters Kluwer Medknow Publications
Citation: Asian Pacific Journal of Tropical Biomedicine. Vol.8, Issue 11 (Nov, 2018), p. 519-526.
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 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.
URI: http://cuir.car.chula.ac.th/handle/123456789/61736
URI: https://doi.org/10.4103/2221-1691.245956
ISSN: 2221-1691 (Print)
2588-9222 (Online)
metadata.dc.identifier.DOI: 10.4103/2221-1691.245956
Type: Article
Appears in Collections:Chula Scholars - 2018

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