哈卡特
小干扰RNA
分子生物学
车站3
RNA干扰
信号转导
干扰素
细胞培养
基因沉默
化学
生物
体外
细胞生物学
转染
生物化学
免疫学
核糖核酸
基因
遗传学
作者
Huan Liu,Yan Wu,Kai Cao,Yuan Xu,Xing Gao,Hong Duo Chen,Long Geng
出处
期刊:PubMed
日期:2015-01-01
卷期号:8 (8): 9202-7
被引量:5
摘要
We hypothesized that interferon-γ (IFN-γ) induces K17 over-expression in HaCaT cells by activating STAT3 and that Sh might inhibit the over-expression through interference of STAT3 signaling.In vitro culture of HaCaT cells treated with IFN-γ and measurement of K17 protein by enzyme linked immunosorbent assay.The level of K17 protein (one kind of keratin protein) in the supernatant induced by IFN-γ was significantly reduced by Shikonin at various concentrations. Interference of STAT3 suppressed the effect of IFN-γ on K17 expression at both mRNA and protein levels. The over-expression of K17 in IFN-γ-induced HaCaT cells was significantly suppressed by 2 µg/L Shikonin. Interfering with STAT3 signaling with 2 µg/L Shikonin resulted in an intermediate level of IFN-γ-induced K17 protein in HaCaT cells.These data demonstrate that IFN-γ induces K17 protein over-expression of HaCaT cells by activating STAT3 and Shikonin may inhibit the over-expression partly through interference of STAT3.
科研通智能强力驱动
Strongly Powered by AbleSci AI