TNF-α enhances the effect of TGF-β on Gli2 expression in the KG-1 leukemic cell line

被引：1
作者：
Li, Zhe [1 ]
Li, Bin [1 ]
Pan, Jing [1 ]
Jin, Jieping [1 ]
机构：
[1] Liaoning Med Coll, Affiliated Hosp 1, Dept Hematol, Jinzhou 121001, Liaoning, Peoples R China
来源：
EXPERIMENTAL AND THERAPEUTIC MEDICINE | 2014年 / 8卷 / 02期
关键词：
Gli family zinc finger 2; transforming growth factor-beta; tumor necrosis factor alpha; specific inhibitor of smad3; TRANSFORMING-GROWTH-FACTOR; HEDGEHOG SIGNALING PATHWAY; SONIC HEDGEHOG; IN-VITRO; MONOCYTIC DIFFERENTIATION; TRANSCRIPTION FACTORS; PROLIFERATION; ACTIVATION; TRANSDUCTION; RESISTANCE;
D O I：
10.3892/etm.2014.1743
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
The Hedgehog (Hh) signaling pathway regulates a variety of tumor-related diseases, including leukemia. The present study aimed to determine whether there was an interaction between the Hh signaling pathway and transforming growth factor (TGF)-beta in the KG-1 cell line. KG-1 cells were treated with TGF-beta, tumor necrosis factor (TNF)-alpha and specific inhibitor of smad3 (SIS3). The expression level of Gli family zinc finger 2 (Gli2) was detected by quantitative polymerase chain reaction (qPCR) and western blot analyses. The results revealed that TGF-beta significantly decreased the expression level of Gli2 in KG-1 cells, and that TNF-alpha and TGF-beta together further reduced Gli2 expression in KG-1 cells. SIS3 inhibited the effect of TGF-beta. These results suggest that Gli2 expression in KG-1 cells is suppressed by TGF-beta in a Smad3-dependent manner, TNF-alpha can enhance the effect of TGF-beta on Gli2 expression and that this occurs independently of Hh receptor signaling.
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页码：676 / 680
页数：5
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