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Background  Golgi protein-73 (GP73) is a Golgi transmembrane glycoprotein elevated in numerous liver diseases. Clinically, GP73 is strongly elevated in the serum of HCC patients and is thus regarded as a novel potential biomarker for HCC. However, the mechanism leading to GP73 dysregulation in liver diseases remains unknown.    Results  This study determined that epithelium-specific ETS (ESE)-1, an epithelium-specific transcription factor, and GP73 expressions were induced by IL-1β stimulation  in vitro , and both were triggered during liver inflammation  in vivo . In hepatocellular carcinoma cells, the overexpression of ESE-1 induced GP73 expression, whereas its knock-down did the opposite. Mechanistically, ESE-1 activated GP73 expression by directly binding to its promoter.    Conclusions  Our findings supported a novel paradigm for ESE-1 as a transcriptional mediator of GP73. This study provided a possible mechanism for GP73 upregulation in liver diseases.    Electronic supplementary material  The online version of this article (doi:10.1186/2045-3701-4-76) contains supplementary material, which is available to authorized users.

Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells