Analysis of the inhibitory mechanism of D-allose on MOLT-4F leukemia cell proliferation.
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.
Hirata
Yuko
Y
Department of Cell Physiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Saito
Madoka
M
Tsukamoto
Ikuko
I
Yamaguchi
Fuminori
F
Sui
Li
L
Kamitori
Kazuyo
K
Dong
Youyi
Y
Uehara
Eisuke
E
Konishi
Ryoji
R
Janjua
Najma
N
Tokuda
Masaaki
M
D002453:Cell Cycle / Q000187:drug effects*; D018797:Cell Cycle Proteins / Q000378:metabolism*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000008:administration & dosage*; D006801:Humans; D007938:Leukemia / Q000378:metabolism* / Q000473:pathology*
D018797:Cell Cycle Proteins; C002055:allose; D005947:Glucose