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The aim of the present study was to investigate the role of the JAK/STAT1signaling pathway in suberoylanilide hydroxamic acid (SAHA)-mediated down-regulationof indoleamine 2,3-dioxygenase (IDO) in gallbladder carcinoma cells. We treatedSGC-996 gallbladder carcinoma cells with IFN-γ and SAHA. Western blotting wasused to detect the expression of IDO, signal transducer and activator of transcription 1(STAT1) phosphorylation and interferon regulatory factor genes-1 (IRF-1). Confocalmicroscopy analysis was used to detect STAT1 translocation. Transient transfectionand reporter gene assay was used for detecting the activation of γ-activated sites(GAS) and interferon-stimulated response elements (ISRE). The results revealedthat IDO was expressed in SGC-996 cells in a dose- and time-dependent manner whenstimulated with IFN-γ and SAHA down-regulated the expression of IDO induced byIFN-γ in a dose-dependent manner. SAHA blocked the expression of IRF-1 inducedby IFN-γ and SAHA inhibited IFN-γ-induced STAT1 phosphorylation and nuclear translocation.In addition, SAHA down-regulated IFN-γ-induced activation of GAS and ISRE. Inconclusion, SAHA down-regulated IDO expression via inhibition of the activationof members of the JAK/STAT1 signaling pathway. Therefore, regulation of the JAK/STAT1signaling pathway may provide a new gallbladder carcinoma immunotherapeutic strategyto break tumor immune tolerance.

SAHA down-regulates the expression of indoleamine 2,3-dioxygenase via inhibition of the JAK/STAT1 signaling pathway in gallbladder carcinoma cells