IFN-γ increased expression of CXCL17 by breast epithelial cells via a JAK-STAT1-dependent pathway
10.3969/j.issn.1007-3969.2015.05.001
- VernacularTitle:IFN-γ通过JAK-STAT1通路诱导乳腺上皮细胞表达趋化因子CXCL17
- Author:
Yajie GUO
;
Zhouluo OU
- Publication Type:Journal Article
- Keywords:
Cytokine;
Chemokine;
IFN-γ;
Breast epithelial cell
- From:
China Oncology
2015;(5):321-325
- CountryChina
- Language:Chinese
-
Abstract:
Background and purpose:There are emerging evidences show that cytokines can mediate the expression and function of chemokines. CXC chemokine ligand 17 (CXCL17) is the latest member in CXC chemokine superfamily, which was identiifed in 2006. It may be involved in anti-tumor immune response. As a mucosal chemokine, CXCL17 was also proved to have anti-inlfammatory and anti-microbial effects. The purpose of this study was to ifgure out which cytokine can impact the expression of CXCL17. Methods:Quantitative real-time PCR (qRT-PCR) was used to detect the mRNA expression of CXCL17 in MCF-10A after cytokines stimulation, such as TNF-α, IL-1β, IFN-γand lipopolysaccharide (LPS). Western blot was used to detect the activation of the JAK-STAT pathway in MCF-10A after IFN-γinduction. Results:All tested cytokines can induce CXCL17 gene expression to varying degrees. However, the effect of IFN-γwas much more powerful by contrast with others. It can enhance the CXCL17 gene expression by about 100-fold. Western blot indicated that IFN-γcan stimulate the expression and phosphorylation of STAT1 in JAK-STAT pathway. Conclusion:Several cytokines can induce the expression of CXCL17 by breast epithelial cells, while IFN-γdramatically increased the expression of it via a JAK-STAT1-dependent pathway. CXCL17 may be the target gene of IFN-γ.
