Analysis of the inhibitory mechanism of D-allose on MOLT-4F leukemia cell proliferation

被引:31
作者
Hirata, Yuko [1 ]
Saito, Madoka [2 ]
Tsukamoto, Ikuko [3 ]
Yamaguchi, Fuminori [1 ]
Sui, Li [3 ]
Kamitori, Kazuyo [1 ]
Dong, Youyi [1 ]
Uehara, Eisuke [1 ]
Konishi, Ryoji [3 ]
Janjua, Najma [4 ]
Tokuda, Masaaki [1 ]
机构
[1] Kagawa Univ, Fac Med, Dept Cell Physiol, Miki, Kagawa 7610793, Japan
[2] Mukogawa Womens Univ, Sch Pharmaceut Sci, Nishinomiya, Hyogo 6638179, Japan
[3] Kagawa Univ, Fac Med, Dept Pharmacobioinformat, Miki, Kagawa 7610793, Japan
[4] Kagawa Prefectural Coll Hlth Sci, Dept Liberal Arts & Sci, Kagawa 7610123, Japan
关键词
D-allose; Rare sugar; Leukemia cell line; Anticancer; TXNIP; REGULATED PROTEIN-1 VDUP1; CARCINOMA CELLS; DEGRADATION; P27(KIP1); GROWTH; CANCER; TXNIP;
D O I
10.1016/j.jbiosc.2008.12.021
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
D-Allose, the C-3 epimer Of D-glucose, is one of the rare sugars found in nature. In the present study, we have elucidated for the first time that various leukemia cell lines have different susceptibility to anti-proliferative activity of D-allose, and that this difference is related to the difference in induction of thioredoxin interacting protein (TXNIP) expression. We examined 5 leukemia cell lines (MOLT-4F, IM-9, HL-60, BALL-1 and Daudi), and found that MOLT-4F (T-cell lymphoblastic leukemia) had the highest susceptibility to D-allose, and that Daudi (Burkitt's lymphoma) had the lowest. D-Allose significantly slowed the cell cycle progression without causing apoptosis of MOLT-4F cells. Intracellular TXNIP expression was specifically and markedly enhanced in MOLT-4F cells by D-allose treatment, and subsequent increase of p27(kip1), a cell cycle inhibitor, was observed. On the other hand, D-allose did not increase TXNIP and p27(kip1) levels at all in Daudi cells. These results indicate that D-allose suppresses MOLT-4F cell proliferation possibly by the inhibition of cell cycle progression via induction of TXNIP expression. (c) 2009, The Society for Biotechnology, Japan. All rights reserved.
引用
收藏
页码:562 / 568
页数:7
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