RT Journal Article
SR Electronic
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
FD International Institute of Anticancer Research
SP 1053
OP 1058
VO 21
IS 6
A1 YUH-TZY LIN
A1 JAI-SING YANG
A1 HUI-JU LIN
A1 TZU-WEI TAN
A1 NOU-YING TANG
A1 JO-HUA CHAING
A1 YUNG-HSIEN CHANG
A1 HSU-FENG LU
A1 JING-GUNG CHUNG
YR 2007
UL http://iv.iiarjournals.org/content/21/6/1053.abstract
AB 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