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ARS Home » Southeast Area » Byron, Georgia » Fruit and Tree Nut Research » Research » Publications at this Location » Publication #257291
Title: Molecular mechanisms involved in the inhibition of MDA-MB-435 breast cancer cells by phenolic acids from the red-flesh peach BY00P6653

Author
item NORATTO, G - Texas A&M University
item CISNEROS-ZEVALLOS, L - Texas A&M University
item BYRNE, D - Texas A&M University
item Okie, William
item PORTER, W - Texas A&M University

Submitted to: Acta horticulturae
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/1/2008
Publication Date: 8/31/2009
Citation: Noratto, G., Cisneros-Zevallos, L., Byrne, D.H., Okie, W.R., Porter, W. 2009. Molecular mechanisms involved in the inhibition of MDA-MB-435 breast cancer cells by phenolic acids from the red-flesh peach BY00P6653. Acta Horticulturae. 841:67-72.

Interpretive Summary: Fruits with highly pigmented flesh are thought to have beneficial health effects. Although not commonly available, peaches exist that have dark red flesh. Extracts from the dark red flesh of peaches bred by ARS-Byron were tested to see their effects on the growth of breast cancer cells in the lab. Results showed inhibition of cell growth by the peach extract. Further work is needed to see if these fruits are beneficial as part of the human diet.

Technical Abstract: A wide variety of fruits and vegetables extracts have been shown to protect against cancer cell growth in vitro. Increasing evidence suggests that phenolics compounds found in fruits and vegetables may have anticancer properties. However, the molecular mechanisms involved in the anti-proliferative activity exerted by these natural compounds are poorly understood. Treatment of the estrogen-negative receptor MDA-MB-435 breast cancer cells with F1, containing mainly chlorogenic acid resulted in a dose-dependent reduction in cell viability with an IC50 = 150 mg chlorogenic acid equiv/L. Concomitantly, F1 treatments led to a time and dose-dependent ERK1/2 phosphorylation, and to a lesser extent c-Jun activation. The early and sustained activation of ERK1/2 was associated with up-regulation of the pro-apoptotic protein Bax. MEK1/2 inhibitor suppressed Bax activation and cytochrome c release from the mitochondria. In conclusion, our studies employing the MEK-MAK inhibitor revealed that prolonged ERK activation by F1 mediated the apoptosis machinery and that MEK-MAK blockage modified the cytotoxicity exerted by F1 through mitochondria permeabilization, indicating that prolonged MEK-MAK activation may be linked to cell death.