α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation
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. D...
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Wolters Kluwer Medknow Publications
2018-01-01
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Series: | Asian Pacific Journal of Tropical Biomedicine |
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Online Access: | http://www.apjtb.org/article.asp?issn=2221-1691;year=2018;volume=8;issue=11;spage=519;epage=526;aulast=Ittiudomrak |
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author | Teeranai Ittiudomrak Songchan Puthong Tanapat Palaga Sittiruk Roytrakul Chanpen Chanchao |
author_facet | Teeranai Ittiudomrak Songchan Puthong Tanapat Palaga Sittiruk Roytrakul Chanpen Chanchao |
author_sort | Teeranai Ittiudomrak |
collection | DOAJ |
description | 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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issn | 2221-1691 |
language | English |
last_indexed | 2024-12-12T10:11:56Z |
publishDate | 2018-01-01 |
publisher | Wolters Kluwer Medknow Publications |
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series | Asian Pacific Journal of Tropical Biomedicine |
spelling | doaj.art-1f2c5d02cfbd46aeba6dd8fef8992fd72022-12-22T00:27:47ZengWolters Kluwer Medknow PublicationsAsian Pacific Journal of Tropical Biomedicine2221-16912018-01-0181151952610.4103/2221-1691.245956α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammationTeeranai IttiudomrakSongchan PuthongTanapat PalagaSittiruk RoytrakulChanpen ChanchaoObjective: 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.http://www.apjtb.org/article.asp?issn=2221-1691;year=2018;volume=8;issue=11;spage=519;epage=526;aulast=Ittiudomrakα-mangostinapigeninbreast cancercell cycle arrestnecrosis |
spellingShingle | Teeranai Ittiudomrak Songchan Puthong Tanapat Palaga Sittiruk Roytrakul Chanpen Chanchao α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation Asian Pacific Journal of Tropical Biomedicine α-mangostin apigenin breast cancer cell cycle arrest necrosis |
title | α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation |
title_full | α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation |
title_fullStr | α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation |
title_full_unstemmed | α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation |
title_short | α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation |
title_sort | α mangostin and apigenin induced the necrotic death of bt474 breast cancer cells with autophagy and inflammation |
topic | α-mangostin apigenin breast cancer cell cycle arrest necrosis |
url | http://www.apjtb.org/article.asp?issn=2221-1691;year=2018;volume=8;issue=11;spage=519;epage=526;aulast=Ittiudomrak |
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