Yang J.-H.Chou C.-C.Cheng Y.-W.Sheen L.-Y.Chou M.-C.Yu H.-S.Wei Y.-H.Chung J.-G.2019-07-112019-07-1120042786915https://scholars.lib.ntu.edu.tw/handle/123456789/413590Apoptosis 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. ? 2004 Elsevier Ltd. All rights reserved.ApoptosisFlow cytometryGlycolic acidHuman leukemia HL-60 cells[SDGs]SDG3antineoplastic agent; benzyloxycarbonylvalylalanylaspartyl fluoromethyl ketone; caspase 3; caspase 8; caspase 9; caspase inhibitor; cyclin A; cyclin B; glycolic acid; antigen expression; apoptosis; article; cancer; cell cycle G2 phase; cell strain HL 60; cell structure; cell viability; concentration response; controlled study; drug effect; drug potency; drug screening; enzyme activation; enzyme activity; flow cytometry; human; human cell; microscopy; signal transduction; Western blotting; Amino Acid Chloromethyl Ketones; Analysis of Variance; Apoptosis; Blotting, Western; Caspase 3; Caspase 9; Caspases; Cell Cycle; Cell Survival; Cyclins; Cysteine Proteinase Inhibitors; DNA; Dose-Response Relationship, Drug; Enzyme Activation; Flow Cytometry; Glycolates; HL-60 Cells; Humans; Indicators and Reagents; Time Factorsjournal article10.1016/j.fct.2004.07.0042-s2.0-4444340999https://www.scopus.com/inward/record.uri?eid=2-s2.0-4444340999&doi=10.1016%2fj.fct.2004.07.004&partnerID=40&md5=8e59a59f23d8fe54eee6514ef1e360ce