Green tea polyphenols induce cell death in breast cancer MCF-7 cells through induction of cell cycle arrest and mitochondrial-mediated apoptosis
Autor: | Huihua Huang, Shi-yi Ou, Shu-min Liu |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Programmed cell death Cell cycle checkpoint Cell Survival Apoptosis DNA Fragmentation Mitochondrion General Biochemistry Genetics and Molecular Biology Article HeLa 03 medical and health sciences 0302 clinical medicine Cell Line Tumor Cytotoxic T cell Humans General Pharmacology Toxicology and Pharmaceutics A549 cell Membrane Potential Mitochondrial General Veterinary biology Tea Caspase 3 Polyphenols General Medicine Cell Cycle Checkpoints Hep G2 Cells biology.organism_classification Flow Cytometry Caspase 9 Chromatin Cell biology Mitochondria 030104 developmental biology MCF-7 A549 Cells 030220 oncology & carcinogenesis MCF-7 Cells Guanosine Triphosphate Reactive Oxygen Species HeLa Cells |
Zdroj: | Journal of Zhejiang University. Science. B. 18(2) |
ISSN: | 1862-1783 |
Popis: | In order to study the molecular mechanisms of green tea polyphenols (GTPs) in treatment or prevention of breast cancer, the cytotoxic effects of GTPs on five human cell lines (MCF-7, A549, Hela, PC3, and HepG2 cells) were determined and the antitumor mechanisms of GTPs in MCF-7 cells were analyzed. The results showed that GTPs exhibited a broad spectrum of inhibition against the detected cancer cell lines, particularly the MCF-7 cells. Studies on the mechanisms revealed that the main modes of cell death induced by GTPs were cell cycle arrest and mitochondrial-mediated apoptosis. Flow cytometric analysis showed that GTPs mediated cell cycle arrest at both G1/M and G2/M transitions. GTP dose dependently led to apoptosis of MCF-7 cells via the mitochondrial pathways, as evidenced by induction of chromatin condensation, reduction of mitochondrial membrane potential (ΔΨ m), improvement in the generation of reactive oxygen species (ROS), induction of DNA fragmentation, and activations of caspase-3 and caspase-9 in the present paper. |
Databáze: | OpenAIRE |
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