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KMID : 1140120070120020106
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Cancer Prevention Research
2007 Volume.12 No. 2 p.106 ~ p.111
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Capsaicin can Induce Apoptosis in Estrogen-sensitive MCF-7 Cells via ERK and p38 MAP-kinases
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Hwang Jin-Taek
Kim Myung-Sunny
Kwon Dae-Young
Kim Hyun-Jin
Sung Mi-Jung
Lee Yun-Kyung
Park Ock-Jin
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Abstract
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Capsaicin is the active component of chili pepper closely associated with prevention of diseases such as diabetes and cancer through modulating cellular signal pathways. To elucidate the involvement of signal pathway in capsaicin-induced apoptosis, it was investigated to test the effect of capsaicin on cancer cell proliferation and cellular signal pathway in MCF-7 human breast cancer cells. Treatment of capsaicin resulted in the inhibition of cell proliferation dose and time-dependently in the cultured cancer cells. This inhibition of growth was expressed by the cleavage of DNA in these cells. The biological consequences of modulating the mitogen-activated protein kinases such as ERK or p38 emerge as a therapeutic target or prevention of human disease such as metabolic syndrome and some cancers. Unveiling the potential
of capsaicin in cytotoxicity via apoptosis as a consequence of the modulation of these cellular stress response proteins can predict therapeutic capability of capsaicin in breast cancers. We have found that the reduction of growth was accompanied with an activation of ERK and p38 in MCF-7 breast cancer cells, which may have caused increased cell apoptosis. This cellular signal transduction events exerted by capsaicin may provide important insights into efficacy of natural chemopreventive compounds found in our diet like capsaicin. (Cancer Prev Res 12, 106-111, 2007)
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KEYWORD
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Capsaicin, Modulation of signal transduction pathway, Mitogen-activated protein kinases, Estrogen-sensitive MCF-7 breast cancer cells
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