Ellagic acid induces apoptosis in TSGH8301 human bladder cancer cells through the endoplasmic reticulum stress‐ and mitochondria‐dependent signaling pathways. Issue 11 (30th March 2013)

• Record Type: Journal Article
• Authors: Ho, Chin‐Chih; Huang, An‐Cheng; Yu, Chun‐Shu; Lien, Jin‐Cherng; Wu, Shin‐Hwar; Huang, Yi‐Ping; Huang, Hui‐Ying; Kuo, Jehn‐Hwa; Liao, Wen‐Yen; Yang, Jai‐Sing; Chen, Po‐Yuan; Chung, Jing‐Gung
• Is Part Of: Environmental toxicology. Volume 29:Issue 11(2014:Nov.)
• Page Start: 1262
• Page End: 1274
• Publication Date: 2013-03-30
• Subjects: Water quality bioassay -- Periodicals; Water -- Pollution -- Toxicology -- Periodicals; Microbiological assay -- Periodicals; Toxicity testing -- Periodicals; Environmental toxicology -- Periodicals; Environmental Pollution -- Periodicals; Environmental Pollutants -- Periodicals; Environmental Monitoring -- Periodicals; Écotoxicologie -- Périodiques; Pollution -- Périodiques; 615.902
• DOI: 10.1002/tox.21857
• Languages: English
• ISSNs: 1520-4081

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>To investigate the effects of ellagic acid on the growth inhibition of TSGH8301 human bladder cancer cells <italic>in vitro</italic>, cells were incubated with various doses of ellagic acid for different time periods. The phase‐contrast microscope was used for examining and photographing the morphological changes in TSGH8301 cells. Flow cytometric assay was used to measure the percentage of viable cells, cell cycle distribution, apoptotic cells, ROS, mitochondrial membrane potential (Δ<italic>Ψm</italic>), Ca<sup>2+</sup>, caspase‐9 and ‐3 activities in TSGH8301 cells after exposure to ellagic acid. Western blotting was used to examine the changes of cell cycle and apoptosis associated proteins levels. Results indicated that ellagic acid induced morphological changes, decreased the percentage of viable cells through the induction of G0/G1 phase arrest and apoptosis, and also showed that ellagic acid promoted ROS and Ca<sup>2+</sup> productions and decreased the level of Δ<italic>Ψm</italic> and promoted activities of caspase‐9 and ‐3. The induction of apoptosis also confirmed by annexin V staining, comet assay, DAPI staining and DNA gel electrophoresis showed that ellagic acid induced apoptosis and DNA damage in TSGH8301 cells. Western blotting assay showed that ellagic acid promoted p21, p53 and decreased CDC2 and WEE1 for leading to G0/G1 phase arrest and promoting BAD expression, AIF and Endo G, cytochrome <italic>c</italic>, caspase‐9 and ‐3 for leading to apoptosis in TSGH8301 cells. On the basis of these observations, we suggest that ellagic acid induced cytotoxic effects for causing a decrease in the percentage of viable cells <italic>via</italic> G0/G1 phase arrest and induction of apoptosis in TSGH8301 cells. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1262–1274, 2014.</p> </abstract>