Growth Inhibition Effects of Isoalantolactone on K562/A02 Cells: Caspase‐dependent Apoptotic Pathways,S Phase Arrest,and Downregulation of Bcr/Abl |
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Authors: | Hong Cai Xiuxiang Meng Yuzhong Li Chuihui Yang Yong Liu |
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Affiliation: | 1. Clinical Laboratory, The Second Hospital of Dalian Medical University, , Dalian, 116023 PR China;2. Clinical Laboratory, Shengjing Hospital of China Medical University, , Shenyang, 110004 PR China;3. Department of Laboratory Hematology, College of Laboratory Medicine, Dalian Medical University, , Dalian, 116044 PR China |
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Abstract: | Isoalantolactone, a sesquiterpene lactone, is the active component of Inula helenium (Compositae). It has been reported that isoalantolactone has the capacity to inhibit tumor cell growth through induction of apoptosis. The purposes of this study were to evaluate the effects of isoalantolactone on the human erythroleukemia drug‐resistant cell line K562/A02 and to provide evidence of its function as a potent therapeutic agent in patients with chronic myelogenous leukemia with the Bcr/Abl phenotype. Our results showed that isoalantolactone significantly inhibited K562/A02 cell growth by downregulating Bcr/Abl expression. Isoalantolactone also induced apoptosis via increase generation of reactive oxygen species, modulation of the protein levels of Bcl‐2 family members, caspase activation, poly ADP‐ribose polymerase (PARP) cleavage, and release of cytochrome c. We also observed that isoalantolactone inhibited proliferation by inducing cell cycle arrest in the S phase. Taken together, all these findings support that growth inhibition effects of isoalantolactone on K562/A02 cells may be mediated through caspase‐dependent apoptotic pathways, S phase arrest, and downregulation of Bcr/Abl. Copyright © 2014 John Wiley & Sons, Ltd. |
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Keywords: | isolantolactone K562/A02 apoptosis Bcr/Abl proliferation |
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