Li Zhe, Li Bin, Pan Jing, Jin Jieping
Department of Hematology, First Affiliated Hospital of Liaoning Medical College, Jinzhou, Liaoning 121001, P.R.China.
Exp Ther Med. 2014 Aug;8(2):676-680. doi: 10.3892/etm.2014.1743. Epub 2014 May 28.
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)-β in the KG-1 cell line. KG-1 cells were treated with TGF-β, tumor necrosis factor (TNF)-α 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-β significantly decreased the expression level of Gli2 in KG-1 cells, and that TNF-α and TGF-β together further reduced Gli2 expression in KG-1 cells. SIS3 inhibited the effect of TGF-β. These results suggest that Gli2 expression in KG-1 cells is suppressed by TGF-β in a Smad3-dependent manner, TNF-α can enhance the effect of TGF-β on Gli2 expression and that this occurs independently of Hh receptor signaling.
刺猬（Hh）信号通路调节包括白血病在内的多种肿瘤相关疾病。本研究旨在确定在KG-1细胞系中，Hh信号通路与转化生长因子（TGF）-β之间是否存在相互作用。用TGF-β、肿瘤坏死因子（TNF）-α和Smad3特异性抑制剂（SIS3）处理KG-1细胞。通过定量聚合酶链反应（qPCR）和蛋白质免疫印迹分析检测Gli家族锌指蛋白2（Gli2）的表达水平。结果显示，TGF-β显著降低KG-1细胞中Gli2的表达水平，并且TNF-α与TGF-β共同作用进一步降低了KG-1细胞中Gli2的表达。SIS3抑制了TGF-β的作用。这些结果表明，TGF-β以Smad3依赖的方式抑制KG-1细胞中Gli2的表达，TNF-α可增强TGF-β对Gli2表达的影响，且这一过程独立于Hh受体信号传导。
