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. 2018 May 2;9:411. doi: 10.3389/fphar.2018.00411

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Copyright © 2018 Lee, Hsu, Lee, Lee, Liu, Chiang and Tsai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed model for the anticancer activity of artocarpin in U87 cells. Artocarpin decreased U87 cell viability by inducing apoptosis in a time- and concentration-dependent manner. Artocarpin-induced apoptosis was associated with caspase activation and PARP cleavage. It was mediated by the mitochondrial pathway as indicated by mitochondrial depolarization, cytochrome c release, and downregulation of the antiapoptotic Bcl-2 protein. Artocarpin induced intracellular ROS generation. Intracellular ROS production was apparently essential for mitochondrial pathway activation and apoptosis induction following artocarpin exposure. Oxidative stress caused by artocarpin treatment was associated with Akt- and ERK1/2 activation as indicated by Akt- and ERK1/2 phosphorylation. The ROS generated by artocarpin treatment induced cell death by PI3K/Akt/ERK1/2. These findings suggest that artocarpin is a potential chemotherapeutic agent for GBM treatment.