Hydroxychavicol, a Piper Betle leaf Component, Induces Apoptosis of CML Cells Through Mitochondrial Reactive Oxygen Species-Dependent JNK and Endothelial Nitric Oxide Synthase Activation and Overrides Imatinib Resistance
EPrints@IICB
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Title |
Hydroxychavicol, a Piper Betle leaf Component, Induces Apoptosis of CML Cells Through Mitochondrial Reactive Oxygen Species-Dependent JNK and Endothelial Nitric Oxide Synthase Activation and Overrides Imatinib Resistance
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Creator |
B. Chakraborty, Jayashree
Mahato, Sanjit Kumar Joshi, Kalpana Shinde, Vaibhav Rakshit, Srabanti Biswas, Nabendu Choudhury (Mukherjee), Indrani Mandal, Labanya Ganguly, Dipyaman Chowdhury, Avik Acharya Jaisankar , P Chaudhuri, Utpal Konar, Aditya Roy, Siddhartha Bandyopadhyay, Santu |
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Subject |
Cancer Biology and Inflammatory Disorder Division
Chemistry Structural Biology & Bioinformatics |
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Description |
Alcoholic extract of Piper betle (Piper betle L.) leaves was recently found to induce apoptosis of CML cells expressing wild type and mutated Bcr-Abl with imatinib resistance phenotype. Hydroxychavicol (HCH), a constituent of the alcoholic extract of Piper betle leaves, was evaluated for anti-CML activity. Here, we report that HCH and its analogues induce killing of primary cells in CML patients and leukemic cell lines expressing wild type and mutated Bcr-Abl, including the T315I mutation, with minimal toxicity to normal human peripheral blood mononuclear cells. HCH causes early but transient increase of mitochondria-derived reactive oxygen species. Reactive oxygen species-dependent persistent activation of JNK leads to an increase in endothelial nitric oxide synthasemediated nitric oxide generation. This causes loss of mitochondrial membrane potential, release of cytochrome c from mitochondria, cleavage of caspase 9, 3 and poly-adenosine diphosphate-ribose polymerase leading to apoptosis. One HCH analogue was also effective in vivo in SCID mice against grafts expressing the T315I mutation, although to a lesser extent than grafts expressing wild type Bcr-Abl, without showing significant bodyweight loss. Our data describe the role of JNK-dependent endothelial nitric oxide synthase-mediated nitric oxide for anti-CML activity of HCH and this molecule merits further testing in pre-clinical and clinical settings. |
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Publisher |
Oxford University Press
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Date |
2012
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Type |
Article
PeerReviewed |
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Format |
application/pdf
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Identifier |
http://www.eprints.iicb.res.in/1620/1/Cancer_Science%2C_2012.pdf
B. Chakraborty, Jayashree and Mahato, Sanjit Kumar and Joshi, Kalpana and Shinde, Vaibhav and Rakshit, Srabanti and Biswas, Nabendu and Choudhury (Mukherjee), Indrani and Mandal, Labanya and Ganguly, Dipyaman and Chowdhury, Avik Acharya and Jaisankar , P and Chaudhuri, Utpal and Konar, Aditya and Roy, Siddhartha and Bandyopadhyay, Santu (2012) Hydroxychavicol, a Piper Betle leaf Component, Induces Apoptosis of CML Cells Through Mitochondrial Reactive Oxygen Species-Dependent JNK and Endothelial Nitric Oxide Synthase Activation and Overrides Imatinib Resistance. Cancer Science, 103 (1). pp. 88-99. |
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Relation |
http://dx.doi.org/10.1111/j.1349-7006.2011.02107.x
http://www.eprints.iicb.res.in/1620/ |
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