Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
MetadataShow full item record
CitationWang, Fang, Qi Long, Yu Gong, Longbo Hu, Hong Zhang, Peter Oettgen, and Tao Peng. 2014. “Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells.” Cell & Bioscience 4 (1): 76. doi:10.1186/2045-3701-4-76. http://dx.doi.org/10.1186/2045-3701-4-76.
AbstractBackground: 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.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:13581219
- HMS Scholarly Articles