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Molecules 2018, 23(12), 3092; https://doi.org/10.3390/molecules23123092

Induction of Apoptosis and Cytotoxicity by Raphasatin in Human Breast Adenocarcinoma MCF-7 Cells

1
UPM-MAKNA Cancer Research Laboratory, Institute of Bioscience, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
2
CREA Consiglio per la ricerca in agricoltura e l’analisi dell’economia agrarian, Centro di ricerca Agricoltura e Ambiente (CREA-AA), Via di Corticella 133, 40128 Bologna, Italy
3
Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK
4
Laboratory of Molecular Biomedicine, Institute of Bioscience, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
5
Laboratory of Food Safety and Food Integrity, Institute of Tropical Agriculture and Food Security, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
6
Department of Food Science, Faculty of Food Science and Technology, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
*
Author to whom correspondence should be addressed.
Received: 18 October 2018 / Revised: 13 November 2018 / Accepted: 14 November 2018 / Published: 27 November 2018
(This article belongs to the Section Natural Products Chemistry)
Full-Text   |   PDF [5329 KB, uploaded 27 November 2018]   |  

Abstract

Glucoraphasatin (GRH), a glucosinolate present abundantly in the plants of the Brassicaceae family, is hydrolyzed by myrosinase to raphasatin, which is considered responsible for its cancer chemopreventive activity; however, the underlying mechanisms of action have not been investigated, particularly in human cell lines. The aims of this study are to determine the cytotoxicity of raphasatin, and to evaluate its potential to cause apoptosis and modulate cell cycle arrest in human breast adenocarcinoma MCF-7 cells. The cytotoxicity was determined following incubation of the cells with glucoraphasatin or raphasatin (0–100 µM), for 24, 48, and 72 h. GRH displayed no cytotoxicity as exemplified by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. When myrosinase was added to the incubation system to convert GRH to raphasatin, cytotoxicity was evident. Exposure of the cells to raphasatin stimulated apoptosis, as was exemplified by cell shrinkage, membrane blebbing, chromatin condensation, and nuclear fragmentation. Moreover, using Annexin V-FITC assay, raphasatin induced apoptosis, as witnessed by changes in cellular distribution of cells, at different stages of apoptosis; in addition, raphasatin caused the arrest of the MCF-7 cells at the G2 + M phase. In conclusion, raphasatin demonstrated cancer chemopreventive potential against human breast adenocarcinoma (MCF-7) cells, through induction of apoptosis and cell cycle arrest. View Full-Text
Keywords: glucoraphasatin; raphasatin; glucosinolates; isothiocyanates; human breast adenocarcinoma cell line; cytotoxicity; apoptosis; cell cycle glucoraphasatin; raphasatin; glucosinolates; isothiocyanates; human breast adenocarcinoma cell line; cytotoxicity; apoptosis; cell cycle
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Ibrahim, M.D.; Kntayya, S.B.; Mohd Ain, N.; Iori, R.; Ioannides, C.; Abdull Razis, A.F. Induction of Apoptosis and Cytotoxicity by Raphasatin in Human Breast Adenocarcinoma MCF-7 Cells. Molecules 2018, 23, 3092.

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