Over-expression of Flt3 induces NF-κB pathway and increases the expression of IL-6

被引：43

作者：

Takahashi, S

Harigae, H

Ishii, KK

Inomata, M

Fujiwara, T

Yokoyama, H

Ishizawa, K

Kameoka, J

Licht, JD

Sasaki, T

Kaku, M

机构：

[1] Tohoku Univ, Sch Med, Dept Clin Lab Med, Aoba Ku, Sendai, Miyagi 9808574, Japan

[2] Tohoku Univ, Sch Med, Dept Rheumatol & Hematol, Aoba Ku, Sendai, Miyagi 9808574, Japan

[3] Mt Sinai Sch Med, Dept Med, Div Hematol Oncol, New York, NY 10029 USA

来源：

LEUKEMIA RESEARCH | 2005年 / 29卷 / 08期

基金：

日本学术振兴会;

关键词：

Flt3; Nf-kappa B; IL-6; AML;

D O I：

10.1016/j.leukres.2005.01.008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Activating mutations or over-expression of the Flt3 is prevalent in acute myeloblastic leukemia (AML), associated with activation of Ras/MAP kinase and other signaling pathways. In this study, we addressed the role of Flt3 in the activation of nuclear factor-kappa B (NF-kappa B); which is a target molecule of these kinase pathways. In BaF3 cells stably expressing 1710, a NF-kappa B-responsive reporter was upregulated and its target gene, IL-6, was increased by the involvement of Flt3-ERK/MAPK-NF-kappa B pathway. Furthermore, we found a modest positive correlation (r = 0.35, p = 0.096) between Flt3 and IL-6 mRNA expression in 24 AML specimens. These results suggest a role of Flt3 overexpression in NF-kappa B pathway. (c) 2005 Elsevier Ltd. All rights reserved.

引用

页码：893 / 899

页数：7

共 27 条

[1] Constitutive NF-κB DNA-binding activity in AML is frequently mediated by a Ras/PI3-K/PKB-dependent pathway [J].