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. 2007 Nov;43(17):2590-601.
doi: 10.1016/j.ejca.2007.08.015. Epub 2007 Oct 1.

beta-Carotene induces apoptosis and up-regulates peroxisome proliferator-activated receptor gamma expression and reactive oxygen species production in MCF-7 cancer cells

Yanhong Cui  1 , Zhongbing Lu, Lin Bai, Zhenhua Shi, Wen-En Zhao, Baolu Zhao
Affiliations

beta-Carotene induces apoptosis and up-regulates peroxisome proliferator-activated receptor gamma expression and reactive oxygen species production in MCF-7 cancer cells

Yanhong Cui et al. Eur J Cancer. 2007 Nov.

Abstract

Although the pharmacological role of beta-carotene in the prevention and treatment of many cancer cells has received increasing attention, the molecular mechanisms underlying such chemopreventive activity are not clear. Since peroxisome proliferator-activated receptor gamma (PPAR-gamma) has been implicated in regulating breast cancer cell differentiation and apoptosis, the effects of beta-carotene on the PPAR-gamma-mediated pathway and its association with reactive oxygen species production in MCF-7 cells were investigated in the present study. The results demonstrated that beta-carotene significantly increased PPAR-gamma mRNA and protein levels in time-dependent manner. In addition, beta-carotene increased the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) expression and decreased the prostanoid synthesis rate-limiting enzyme cyclooxygenase-2 expression. 2-chloro-5-nitro-N-phenylbenzamide (GW9662), an irreversible PPAR-gamma antagonist, partly attenuated the cell death caused by beta-carotene. Further, reactive oxygen species (ROS) production was induced by beta-carotene, resulting in mitochondrial dysfunction and cytochrome C release. Reduced glutathione (GSH) treatment decreases the intracellular ROS and prevents cytochrome C release and cell apoptosis induced by beta-carotene. In total, these observations suggest that the synergistic effect of PPAR-gamma expression and ROS production may account for beta-carotene-mediated anticancer activities.

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