Abstract
Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide), a major pungent ingredient in a variety of red peppers of the genus Capsicum, is a type of vanilloids. It has been shown to exert biological activities in many cancer cell lines. It was found that capsaicin induces dose-dependent growth inhibition of MCF-7 cells, which do not express caspase-3. In this study, we investigated the molecular mechanism of capsaicin-induced apoptosis in MCF-7 cells. Treatment with capsaicin for 24 hours resulted in a dose-dependent apoptosis in MCF-7 cells. After addition of capsaicin, levels of reactive oxygen species (ROS) reduced slightly in the earlier time of treatment. Interestingly, an elevation of intracellular calcium ion (Ca2+) concentration was also detected in MCF-7 cells. It is worth noting that apoptosis-inducing factor (AIF) translocated into the cytosol and nucleus from mitochondria, suggesting that capsaicin may induce cellular apoptosis through caspase-independent pathway in MCF-7 cells. Furthermore, capsaicin may directly enter the cell or penetrate cell membrane to induce cell death and the expression of TRPV1 could increase the sensitivity of capsaicin for cells. Hence, capsaicin may be a potent drug in breast cancer therapy.
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