Molecular mechanisms of methylsulfonylmethane and allicin in the inhibition of CD44(+/-) breast cancer cells growth
dc.contributor.author | Sarkhani, E | |
dc.contributor.author | Najafzadeh, N | |
dc.contributor.author | Tata, N | |
dc.contributor.author | Dastan, M | |
dc.contributor.author | Mazani, M | |
dc.contributor.author | Arzanlou, M | |
dc.date.accessioned | 2018-08-26T07:13:49Z | |
dc.date.available | 2018-08-26T07:13:49Z | |
dc.date.issued | 2017 | |
dc.identifier.uri | http://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/45033 | |
dc.description.abstract | Breast carcinoma is a common cause of cancer death in women worldwide. CD44(+/-) cells were isolated from MCF7 cell line by magnetic-activated cell sorting (MACS) and treated with methylsulfonylmethane (MSM), allicin, and the combination of them. The cytotoxicity and cell cycle arrest were measured using MIT assay and flow cytometry. Moreover, mRNA levels of apoptosis regulators Bax, p53, and caspase-3 were measured using reverse transcriptase-polymerase chain reaction (RT-PCR). The combination treatment inhibited CD44(-) and CD44(+) cells in the G2/M and S phases of the cell cycle, respectively. Importantly, Box expression was significantly higher in the MSM allicin-treated CD44(+) cells than in the MSM- or allicin-treated cells (P < .05). The combination treatment enhanced more caspase-3 mRNA expression than allicin alone in both CD44(+/-) cells. Taken together, the combination treatment with MSM and allicin mediated cytotoxicity through modulating the expression of the key apoptotic factors. (C) 2017 Elsevier Ltd. All rights reserved. | |
dc.language.iso | English | |
dc.relation.ispartof | JOURNAL OF FUNCTIONAL FOODS | |
dc.subject | CD44 | |
dc.subject | Breast carcinoma | |
dc.subject | Allicin | |
dc.subject | Methylsulfonylmethane | |
dc.subject | Apoptosis | |
dc.subject | Cell cycle arrest | |
dc.title | Molecular mechanisms of methylsulfonylmethane and allicin in the inhibition of CD44(+/-) breast cancer cells growth | |
dc.type | Article | |
dc.citation.volume | 39 | |
dc.citation.spage | 50 | |
dc.citation.epage | 57 | |
dc.citation.index | Web of science | |
dc.identifier.DOI | https://doi.org/10.1016/j.jff.2017.10.007 |
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