1. Licochalcone A-induced human bladder cancer T24 cells apoptosis triggered by mitochondria dysfunction and endoplasmic reticulum stress
- Author
-
Xuan Yuan, Hong Zhao, Defang Li, Jiangtao Jiang, Qiusheng Zheng, Penglong Wang, Xiling Sun, and Xiaoyi Ma
- Subjects
Mitochondrial ROS ,Licochalcone A ,Article Subject ,genetic structures ,lcsh:Medicine ,Apoptosis ,Biology ,Mitochondrion ,medicine.disease_cause ,General Biochemistry, Genetics and Molecular Biology ,chemistry.chemical_compound ,Chalcones ,Cell Line, Tumor ,medicine ,Humans ,HSP70 Heat-Shock Proteins ,Cell Proliferation ,chemistry.chemical_classification ,Reactive oxygen species ,General Immunology and Microbiology ,Endoplasmic reticulum ,lcsh:R ,Membrane Proteins ,General Medicine ,Endoplasmic Reticulum Stress ,eye diseases ,Cell biology ,Mitochondria ,Oxidative Stress ,chemistry ,Urinary Bladder Neoplasms ,Signal transduction ,Reactive Oxygen Species ,Oxidative stress ,Signal Transduction ,Research Article - Abstract
Licochalcone A (LCA), a licorice chalconoid, is considered to be a bioactive agent with chemopreventive potential. This study investigated the mechanisms involved in LCA-induced apoptosis in human bladder cancer T24 cells. LCA significantly inhibited cells proliferation, increased reactive oxygen species (ROS) levels, and caused T24 cells apoptosis. Moreover, LCA induced mitochondrial dysfunction, caspase-3 activation, and poly-ADP-ribose polymerase (PARP) cleavage, which displayed features of mitochondria-dependent apoptotic signals. Besides, exposure of T24 cells to LCA triggered endoplasmic reticulum (ER) stress; as indicated by the enhancement in 78 kDa glucose-regulated protein (GRP 78), growth arrest and DNA damage-inducible gene 153/C/EBP homology protein (GADD153/CHOP) expression, ER stress-dependent apoptosis is caused by the activation of ER-specific caspase-12. All the findings from our study suggest that LCA initiates mitochondrial ROS generation and induces oxidative stress that consequently causes T24 cell apoptosis via the mitochondria-dependent and the ER stress-triggered signaling pathways.
- Published
- 2013