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Kim et al. BMC Cancer (2016) 16:452 DOI 10.1186/s12885-016-2516-RESEARCH ARTICLEOpen AccessSilibinin induces mitochondrial NOX4mediated endoplasmic reticulum stress response and its subsequent apoptosisSang-Hun Kim1, Kwang-Youn Kim2, Sun-Nyoung Yu1,3, Young-Kyo Seo2, Sung-Sik Chun4, Hak-Sun Yu3,5 and Soon-Cheol Ahn1,3*AbstractBackground: Silibinin, a biologically active compound of milk thistle, has chemopreventive effects on cancer cell lines. Recently it was reported that silibinin inhibited tumor growth through activation of the apoptotic signaling pathway. Although various evidences showed multiple signaling pathways of silibinin in apoptosis, there were no reports to address the clear mechanism of ROS-mediated pathway in prostate cancer PC-3 cells. Several studies suggested that reactive oxygen species (ROS) play an important role in various signaling cascades, but the primary source of ROS was currently unclear. Methods: The effect of silibinin was investigated on cell growth of prostate cell lines by MTT assay. We examined whether silibinin induced apoptosis through production of ROS using flow cytometry. Expression of apoptosis-, endoplasmic reticulum (ER)-related protein and gene were determined by western blotting and RT-PCR, respectively. Results: Results showed that silibinin triggered mitochondrial ROS production through NOX4 expression and finally led to induce apoptosis. In addition, mitochondrial ROS caused ER stress through disruption of Ca2+ homeostasis. Co-treatment of ROS inhibitor reduced the silibinin-induced apoptosis throu.
