title: Shikonin inhibits IFN-γ-induced K17 over-expression of HaCaT cells by interfering with STAT3 signaling.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China ; Department of Dermatology, Hospital of Beihua University Jilin, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wu
authors.affiliation: HLA Laboratory Pathology/Laboratory Medicine, University of Texas, Anderson Cancer Center 8515 Fannin St, Houston, TX 77054, USA.
authors.forename: Kai
authors.initials: K
authors.lastname: Cao
authors.affiliation: Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China.
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Xu
authors.affiliation: Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China.
authors.forename: Xing-Hua
authors.initials: XH
authors.lastname: Gao
authors.affiliation: Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China.
authors.forename: Hong-Duo
authors.initials: HD
authors.lastname: Chen
authors.affiliation: Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China.
authors.forename: Long
authors.initials: L
authors.lastname: Geng
mesh_terms: D002460:Cell Line; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology*; D053537:Keratin-17 / Q000378:metabolism*; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism; D009285:Naphthoquinones / Q000494:pharmacology*; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D053537:Keratin-17; D009285:Naphthoquinones; D050796:STAT3 Transcription Factor; C016101:shikonin; D007371:Interferon-gamma
keywords: IFN-γ; K17; STAT3; Shikonin