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Title :A modified version of galectin-9 induces cell cycle arrest and apoptosis of Burkitt and Hodgkin lymphoma cells
Authors :Makishi, Shoko
Okudaira, Takeo
Ishikawa, Chie
Sawada, Shigeki
Watanabe, Toshiki
Hirashima, Mitsuomi
Sunakawa, Hajime
Mori, Naoki
Issue Date :May-2008
Abstract :Identification of galectin-9 as a ligand for T-cell immunoglobulin- and mucin-domain-containing molecule-3 (Tim-3), expressed on Th1 cells, has established the Tim-3-galectin-9 pathway as a regulator of Th1 immunity. Whereas there is compelling evidence for the effects of galectin-9 on T-cell fate, limited information is available on the impact of galectin-9 on B lymphocytes. We found that protease-resistant galectin-9, hG9NC(null), but not galectin-1 or -8, prevented cell growth of malignant B cells such as Burkitt lymphoma (BL) and Hodgkin lymphoma (HL). β-galactoside binding was essential for galectin-9-induced cell growth suppression. hG9NC(null) induced cell cycle arrest by reducing the expression of cyclin D1, D2, B1, Cdk4, Cdc25C and c-Myc, and apoptosis by reducing the expression of XIAP, c-IAP2 and survivin. Most of these genes are regulated by nuclear factor-κB (NF-κB), and constitutive activation of NF-κB is a common characteristic of both types of malignancies. hG9NC(null) inhibited IκBα phosphorylation, resulting in suppression of NF-κB. AP-1 has also been implicated in the control of cell survival. hG9NC(null) inhibited the expression of JunD, resulting in the suppression of AP-1. Our results suggest that hG9NC(null) is a potentially suitable agent for the management of BL and HL.
URL :http://www3.interscience.wiley.com/journal/120120074/abstract
Type Local :雑誌掲載論文
ISSN :0007-1048
Publisher :Blackwell Publishing
URI :http://hdl.handle.net/20.500.12000/10319
Citation :British journal of haematology Vol.142 no.4 p.583 -594
Appears in Collections:Peer-reviewed Journal Articles (Faculty of Medicine)

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