Baicalein induced cell cycle arrest and apoptosis in human lung squamous carcinoma CH27 cells

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Title:	Baicalein induced cell cycle arrest and apoptosis in human lung squamous carcinoma CH27 cells
Authors:	Lee, HZ;Leung, HWC;Lai, MY;Wu, CH
Contributors:	藥學院藥化所;China Med Univ, Grad Inst Pharmaceut Chem, Taichung 40402, Taiwan;China Med Univ, Sch Pharm, Taichung 40402, Taiwan;Chi Mei Med Ctr, Dept Radiat Oncol, Tainan, Taiwan
Date:	2005
Issue Date:	2010-09-24 15:09:39 (UTC+8)
Publisher:	INT INST ANTICANCER RESEARCH
Abstract:	It is well known that dietary phenolic compounds can elicit vital cellular responses such as cytotoxicity, cell cycle arrest and apoptosis by activating a cascade of molecular events. Ellagic acid is one of these phenolic compounds, but the exact mechanism of its action is still unclear. The objective of this study was to investigate ellagic acid-induced cell cycle arrest and apoptosis in T24 human bladder cancer cells in vitro. Assays were performed to determine cell viability, cell cycle arrest, apoptosis, caspases-3 activity and gene expression, measured by flow cytometric assay, polymerase chain reaction (PCR) and determination of caspase-3 activity. Ellagic acid significantly reduced the viable cells, induced G0/G1-phase arrest of the cell cycle and apoptosis. Ellagic acid also increased p53 and p21 and decreased CDK2 gene expression, that may lead to the G0/G1 arrest of T24 cells. Ellagic acid also promoted caspase-3 activity after exposure for 1, 3, 6, 12 and 24 h, which led to induction of apoptosis. Furthermore, the ellagic acid-induced apoptosis on T24 cells was blocked by the broad-spectrum caspase inhibitor (z-VAD-fmk).
Relation:	ANTICANCER RESEARCH 25(2A):959-964
Appears in Collections:	[Graduate Institute of Pharmaceutical Chemistry] Journal articles

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