Abstract
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.
Highlights
The Hedgehog (Hh) signaling pathway is linked to cell growth and differentiation
To determine whether transforming growth factor (TGF)‐β or tumor necrosis factor (TNF)‐α affected the expression level of Gli family zinc finger 2 (Gli2), KG‐1 cells were incubated with TGF‐β, with TNF‐α or without either
A significant reduction in the expression level of Gli2 mRNA in response to TGF‐β was observed in the KG‐1 cells (Fig. 1A)
Summary
The Hedgehog (Hh) signaling pathway is linked to cell growth and differentiation. It is involved in embryonic pattern formation and adult tissue homeostasis [1]. The Hh signaling pathway has been revealed to be dysregulated in several human malignancies and to be critical for the maintenance and expansion of malignant stem cells [2]. Gli family zinc finger (Gli) transcription factors constitute the final effectors of the Hh signaling pathway. In a number of tumors, including those of the pancreas, prostate, skin or lungs, the ectopic activation of Gli proteins has been linked to tumorigenesis [3]. There has been evidence suggesting additional, noncanonical mechanisms of Gli activation [3]. Certain studies have suggested that in normal fibroblasts and keratinocytes, as well
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