1. Induction of apoptosis and G2/M arrest by ampelopsin E from Dryobalanops towards triple negative breast cancer cells, MDA-MB-231
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Yong Sze Ong, Jhi Biau Foo, Swee Kong Yeap, Yin Sim Tor, Napsiah Abd Rahman, Norizan Ahmat, Agustono Wibowo, Zainal Abidin Razali, Sharida Fakurazi, and Latifah Saiful Yazan
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0301 basic medicine ,Programmed cell death ,Cell cycle checkpoint ,Cytotoxicity ,Apoptosis ,Triple Negative Breast Neoplasms ,Cell cycle arrest ,HeLa ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Cell Line, Tumor ,Humans ,Medicine ,Cytotoxic T cell ,MTT assay ,Viability assay ,Dryobalanops sp ,Flavonoids ,biology ,Plant Extracts ,business.industry ,Cell Cycle Checkpoints ,General Medicine ,biology.organism_classification ,Molecular biology ,Dipterocarpaceae ,Ampelopsin ,030104 developmental biology ,Complementary and alternative medicine ,chemistry ,030220 oncology & carcinogenesis ,Immunology ,Ampelopsin E ,business ,Research Article - Abstract
Background Several compounds isolated from Dryobalanops have been reported to exhibit cytotoxic effects to several cancer cell lines. This study investigated the cytotoxic effects, cell cycle arrest and mode of cell death in ampelopsin E-treated triple negative cells, MDA-MB-231. Methods Cytotoxicity of ampelopsin E, ampelopsin F, flexuosol A, laevifonol, Malaysianol A, Malaysianol D and nepalensinol E isolated from Dryobalanops towards human colon cancer HT-29, breast cancer MDA-MB-231 and MCF-7, alveolar carcinoma HeLa and mouse embryonic fibroblast NIH/3 T3 cells were determined by MTT assay. The cells were treated with the compounds (0.94–30 μM) for 72 h. The mode of cell death was evaluated by using an inverted light microscope and annexin V/PI analysis. Cell cycle analysis was performed by using a flow cytometer. Results Data showed that ampelopsin E was most cytotoxic toward MDA-MB-231 with the IC50 (50 % inhibition of cell viability compared to control) of 14.5 ± 0.71 μM at 72 h. Cell shrinkage, membrane blebbing and formation apoptotic bodies characteristic of apoptosis were observed following treatment with ampelopsin E. The annexin V/PI flow cytometric analysis further confirmed that ampelopsin E induced apoptosis in MDA-MB-231 cells. Cell cycle analysis revealed that ampelopsin E induced G2/M phase cell cycle arrest in the cells. Conclusion Ampelopsin E induced apoptosis and cell cycle arrest in MDA-MB-231 cells. Therefore, ampelopsin E has the potential to be developed into an anticancer agent for treatment of triple negative breast cancer.
- Published
- 2016
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