2008年8月
A modified version of galectin-9 induces cell cycle arrest and apoptosis of Burkitt and Hodgkin lymphoma cells (Retracted article. See vol. 152, pg. 788, 2011)
BRITISH JOURNAL OF HAEMATOLOGY
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- 巻
- 142
- 号
- 4
- 開始ページ
- 583
- 終了ページ
- 594
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1111/j.1365-2141.2008.07229.x
- 出版者・発行元
- WILEY
The identification of galectin-9 as a ligand for T-cell immunoglobulin- and mucin-domain-containing molecule-3 (Tim-3), expressed on T-helper type-1 (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). beta-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 the genes that encode these proteins are regulated by nuclear factor-kappa B (NF-kappa B), and constitutive activation of NF-kappa Beta is a common characteristic of both types of malignancies. hG9NC(null) inhibited I kappa B alpha phosphorylation, resulting in suppression of NF-kappa B. 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.
- リンク情報
- ID情報
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- DOI : 10.1111/j.1365-2141.2008.07229.x
- ISSN : 0007-1048
- eISSN : 1365-2141
- Web of Science ID : WOS:000257796800008