Lili Liu1, Yan Wu2, Kai Cao3, Yuan-Yuan Xu2, Xing-Hua Gao2, Hong-Duo Chen2, Long Geng2. 1. Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China ; Department of Dermatology, Hospital of Beihua University Jilin, China. 2. Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China. 3. HLA Laboratory Pathology/Laboratory Medicine, University of Texas, Anderson Cancer Center 8515 Fannin St, Houston, TX 77054, USA.
Abstract
OBJECTIVES: 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. METHODS: In vitro culture of HaCaT cells treated with IFN-γ and measurement of K17 protein by enzyme linked immunosorbent assay. RESULTS: 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. CONCLUSIONS: 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.
OBJECTIVES: 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. METHODS: In vitro culture of HaCaT cells treated with IFN-γ and measurement of K17 protein by enzyme linked immunosorbent assay. RESULTS: 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. CONCLUSIONS: 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.
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