TY - JOUR T1 - Baicalein Induces Apoptosis in SCC-4 Human Tongue Cancer Cells <em>via</em> a Ca<sup>2+</sup>-dependent Mitochondrial Pathway JF - In Vivo JO - In Vivo SP - 1053 LP - 1058 VL - 21 IS - 6 AU - YUH-TZY LIN AU - JAI-SING YANG AU - HUI-JU LIN AU - TZU-WEI TAN AU - NOU-YING TANG AU - JO-HUA CHAING AU - YUNG-HSIEN CHANG AU - HSU-FENG LU AU - JING-GUNG CHUNG Y1 - 2007/11/01 UR - http://iv.iiarjournals.org/content/21/6/1053.abstract N2 - Background: The effects of baicalein on SCC-4 human tongue cancer cells were examined to better understand its effect on apoptosis and associated possible signal pathways in vitro. Materials and Methods: Apoptosis induction, reactive oxygen species (ROS), cytoplasmic Ca2+, mitochondrial membrane potential (MMP) and caspase-3 activity were analyzed using the flow cytometric assay. Apoptosis-associated proteins, such as p53, BAX, BCL-2, cytochrome c, caspase-3 and -9, EndoG and AIF were determined by Western blotting. Results: Our results showed that baicalein promoted the levels of p53, BAX, cytochrome c, capase-3 and -9 and reduced the level of BCL-2, which were associated with the induction of apoptotic cell death of SCC-4 cells. A release of cytochrome c from mitochondria into cytosol was demonstrated and an activation of caspase-3, which led to the occurrence of apoptosis in SCC-4 cells treated with baicalein as determined by Western blot. In order to understand the role of Ca2+ in the induction of apoptosis, cells were pre-treated with BAPTA (intracellular calcium chelator) and baicalein. It was shown that the MMP was restored, and the level of cytoplasmic Ca2+ suppressed, the proportion of cells undergoing apoptosis was also markedly diminished. Our data suggest that cellular Ca2+ modulates baicalein-induced cell death via a Ca2+-dependent mitochondrial death pathway in SCC-4 cells. Copyright © 2007 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved ER -