|Title:||EFFECTS OF GLYCOLIC ACID ON THE INDUCTION OF APOPTOSIS VIA CASPASE-3 ACTIVATION IN HUMAN LEUKEMIA CELL LINE (HL-60)||Authors:||YANG, JEN-HUNG
|Keywords:||glycolic acid;human leukemia HL-60 cells;apoptosis;flow cytometry||Issue Date:||2004||Journal Volume:||v.42||Journal Issue:||n.11||Start page/Pages:||1777-1784||Source:||FOOD AND CHEMICAL TOXICOLOGY||Abstract:||
Apoptosis is a particular process that leads to the programmed cell death, and it has been a potentially therapeutic target of cancer. In this study, we evaluated the possible apoptotic effects of glycolic acid on human leukemia cell line (HL-60) in vitro. The morphological changes, cell viability, apoptosis induction, and caspase-3 activity were measured by phase microscopy, flow cytometry, and Western blot analysis. Morphological changes including shrinkage of cells were clearly demonstrated in HL-60 cells treated with increasing concentrations of glycolic acid. Cell viability was significantly affected by glycolic acid treatment in a dose- and time-dependent manner. In comparison to the control group, glycolic acid treatment had a profound effect in the induction of apoptosis by flow cytometric assays. In the cell cycle analysis, glycolic acid caused the increased percentage of cells in G2/M phase and the decreased expression of the cyclin A and cyclin B1, suggesting the induction of G2/M arrest of cell cycle by glycolic acid. Moreover, glycolic acid treatment promoted caspase-9 and -3 activity in a dose-dependent manner, but caspse-8 activity was not affected during the same process. Glycolic acid co-administrated with broad-spectrum caspase inhibitor, z-VAD-fmk, caspase-3 activity was blunted and apoptosis was also markedly blocked in HL-60 cells. In conclusion, glycolic acid-induced apoptosis in HL-60 cells may be through the activation of caspase-3. Future studies focusing on cell signaling and biological significance of glycolic acid-induced apoptosis would lead to exploring the mechanisms of chemotherapeutic potency of glycolic acid in human cancers. (C) 2004 Elsevier Ltd. All rights reserved.
|Appears in Collections:||健康政策與管理研究所|
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.