SEARCH:   Advanced

Blood, 15 October 2004, Vol. 104, No. 8, pp. 2514-2522. Prepublished online as a Blood First Edition Paper on June 29, 2004; DOI 10.1182/blood-2003-11-4065. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-11-4065v1 104/8/2514    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bandyopadhyay, G. Articles by Bandyopadhyay, S. Search for Related Content PubMed PubMed Citation Articles by Bandyopadhyay, G. Articles by Bandyopadhyay, S. Related Collections Neoplasia Apoptosis Oncogenes and Tumor Suppressors Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Chlorogenic acid inhibits Bcr-Abl tyrosine kinase and triggers p38 mitogen-activated protein kinase–dependent apoptosis in chronic myelogenous leukemic cells Gautam Bandyopadhyay, Tanusree Biswas, Keshab C. Roy, Swapan Mandal, Chhabinath Mandal, Bikas C. Pal, Samir Bhattacharya, Srabanti Rakshit, Dilip K. Bhattacharya, Utpal Chaudhuri, Aditya Konar, and Santu Bandyopadhyay From the Indian Institute of Chemical Biology, Kolkata, India; Vivekananda Institute of Medical Sciences, Kolkata, India; and the Institute of Haematology and Transfusion Medicine, Medical College, Kolkata, India. We report that chlorogenic acid (Chl) induces apoptosis of several Bcr-Abl–positive chronic myelogenous leukemia (CML) cell lines and primary cells from CML patients in vitro and destroys Bcr-Abl–positive K562 cells in vivo. In contrast, this compound has no effect on the growth and viability of Bcr-Abl–negative lymphocytic and myeloid cell lines and primary CML cells. Sodium chlorogenate (NaChl) exhibits 2-fold higher efficiency in killing K562 cells compared with Chl. NaChl also induces growth inhibition of squamous cell carcinoma (HSC-2) and salivary gland tumor cells (HSG), although at 50-fold higher concentration. NaChl inhibits autophosphorylation of p210Bcr-Abl fusion protein rapidly. We demonstrate that p38 phosphorylation is increased in Bcr-Abl–positive cells after treatment with NaChl and closely paralleled the inhibition of Bcr-Abl phosphorylation. NaChl did not increase phosphorylation of p38 in Bcr-Abl–negative cells including HSC-2 and HSG that are responsive to this compound, indicating that p38 activation by NaChl is dependent on Bcr-Abl kinase inhibition. Inhibition of p38 activity by SB203580 significantly reduced NaChl-induced apoptosis of K562 cells, whereas activation of p38 by anisomycin augmented the apoptosis. These findings indicate that inhibition of Bcr-Abl kinase leading to activation of p38 mitogen-activated protein (MAP) kinase may play an important role in the anti-CML activity of Chl. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J.-C. Currie, S. Fortier, A. Sina, J. Galipeau, J. Cao, and B. Annabi MT1-MMP Down-regulates the Glucose 6-Phosphate Transporter Expression in Marrow Stromal Cells: A MOLECULAR LINK BETWEEN PRO-MMP-2 ACTIVATION, CHEMOTAXIS, AND CELL SURVIVAL J. Biol. Chem., March 16, 2007; 282(11): 8142 - 8149. [Abstract] [Full Text] [PDF]

	Copyright © 2004 by American Society of Hematology         Online ISSN: 1528-0020