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Capsaicin-lnduced apoptosis of h-ras-transformed human breast epithelial cells is rac-dependentvia ros generation

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Abstract

Many studies have focused on the anticarcinogenic, antimutagenic or chemopreventive activities of capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) which is a major pungent ingredient in red pepper. We have previously shown that capsaicin selectively induces apoptosis in H-ras-transformed MCF10A human breast epithelial cells but not in their normal cell counterparts (Int. J. Cancer, 103, 475-482, 2003). In this study, we investigated the possible roles of reactive oxygen species (ROS) and Rac1 in capsaicin-induced apoptosis of H-ras MCF10A cells. Selective induction of ROS generation by capsaicin treatment was observed only in H-ras MCF10A cells. Pretreatment of H-ras MCF10A cells with an antioxidant N-acetylcysteine (NAC) significantly reversed capsaicin-induced growth inhibition, suggesting that ROS may mediate the apoptosis of H-ras-transformed cells induced by capsaicin. Rac1 was prominently activated by H-ras in MCF10A cells. Based on the studies using a wild type Rac1 and a dominant negative Rad constructs, we propose that Rac1 activity is critical for inhibitory effect of capsaicin on growth of H-ras-transformed MCF10A cells possibly through ROS generation.

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Correspondence to Aree Moon.

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Kim, S., Moon, A. Capsaicin-lnduced apoptosis of h-ras-transformed human breast epithelial cells is rac-dependentvia ros generation. Arch Pharm Res 27, 845–849 (2004). https://doi.org/10.1007/BF02980177

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