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

α-Mangostin and apigenin induced the necrotic death of BT474 breast cancer cells with autophagy and inflammation
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摘要 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: 毩-Mangostin and apigenin were reported in comparison to doxorubicin, a chemotherapeutic drug. Ductal carcinoma(BT474) cell line and nontumorigenic epithelial tissue from mammary gland(MCF-10 A) 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 observed using propidium iodide st桋 and propidium iodide staining while cell-cycle arrest wasaining. 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 and apigenin were more cytotoxic to BT474 cells. Longer exposure times to 毩-mangostin enin caused more floating cells and a lower density of adhered cells wi毩-mangostin and apigth more vacuoles present in the colonies in BT474 only. 毩-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, 毩-mangostin and apigenin arrested the cellcycle 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, autophagyassociated and apoptosis-associated genes. Conclusions: ntial new sources of chemotherapeuti毩-Mangostin and apigenin are worth investigating as potec agents for breast cancer treatment. 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: 毩-Mangostin and apigenin were reported in comparison to doxorubicin, a chemotherapeutic drug. Ductal carcinoma(BT474) cell line and nontumorigenic epithelial tissue from mammary gland(MCF-10 A) 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 observed using propidium iodide st桋 and propidium iodide staining while cell-cycle arrest wasaining. 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 and apigenin were more cytotoxic to BT474 cells. Longer exposure times to 毩-mangostin enin caused more floating cells and a lower density of adhered cells wi毩-mangostin and apigth more vacuoles present in the colonies in BT474 only. 毩-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, 毩-mangostin and apigenin arrested the cellcycle 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, autophagyassociated and apoptosis-associated genes. Conclusions: ntial new sources of chemotherapeuti毩-Mangostin and apigenin are worth investigating as potec agents for breast cancer treatment.
出处 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2018年第11期519-526,共8页 亚太热带生物医学杂志(英文版)
基金 financially supported by Chulalongkorn University the Doctoral Degree Chulalongkorn University 100th Year Birthday Anniversary the 90th Anniversary of Chulalongkorn University Fund(Ratchadaphiseksomphot Endowment Fund) Sci-Super IV_61_003 and the Overseas Research Experience Scholarship for Graduate Student
关键词 α-Mangostin APIGENIN Breast cancer Cell cycle arrest NECROSIS α-Mangostin Apigenin Breast cancer Cell cycle arrest Necrosis
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