Daucus carota pentane-based fractions arrest the cell cycle and increase apoptosis in MDA-MB-231 breast cancer cellsReportar como inadecuado




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BMC Complementary and Alternative Medicine

, 14:387

Basic research

Abstract

BackgroundDaucus carota L.ssp.carota wild carrot, an herb used in folk medicine worldwide, was recently demonstrated to exhibit anticancer activity. In this study we examined the anticancer effect of Daucus carota oil extract DCOE fractions on the human breast adenocarcinoma cell lines MDA-MB-231 and MCF-7 and clarified the mechanism of action.

Methods and resultsUsing the WST assay, the pentane fraction F1 and 1:1 pentane:diethyl ether fraction F2 were shown to possess the highest cytotoxicity against both cell lines. Flow cytometric analysis revealed that both fractions induced the accumulation of cells in the sub-G1 phase, increase in apoptotic cell death and chromatin condensation. The increase in apoptosis in response to treatment was also apparent in the increase in BAX and the decrease in Bcl-2 levels as well as the proteolytic cleavage of both caspase-3 and PARP as revealed by Western blot. Furthermore, treatment of MDA-MB-231 cells with either fraction significantly reduced the level of phosphorylated Erk but did not show any effect on phosphorylated Akt. The combined treatment with a potent PI3K inhibitor wortmannin and F1 or F2 fraction had a synergistic inhibitory effect on cell survival which shows that these two drugs work on different pathways.

ConclusionsThese results suggest that the pentane-based fractions of DCOE possess potential anti-cancer activity that is mainly mediated through the Erk pathway.

KeywordsDaucus carota Breast cancer Proliferation Apoptosis PI3K MAPK Electronic supplementary materialThe online version of this article doi:10.1186-1472-6882-14-387 contains supplementary material, which is available to authorized users.

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Autor: Wassim N Shebaby - Mohammad Mroueh - Kikki Bodman-Smith - Anthony Mansour - Robin I Taleb - Costantine F Daher - Mirvat 

Fuente: https://link.springer.com/







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