Cargando…

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

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Wang, Fang, Long, Qi, Gong, Yu, Hu, Longbo, Zhang, Hong, Oettgen, Peter, Peng, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271417/
https://www.ncbi.nlm.nih.gov/pubmed/25530841
http://dx.doi.org/10.1186/2045-3701-4-76
_version_ 1782349602292236288
author Wang, Fang
Long, Qi
Gong, Yu
Hu, Longbo
Zhang, Hong
Oettgen, Peter
Peng, Tao
author_facet Wang, Fang
Long, Qi
Gong, Yu
Hu, Longbo
Zhang, Hong
Oettgen, Peter
Peng, Tao
author_sort Wang, Fang
collection PubMed
description 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.
format Online
Article
Text
id pubmed-4271417
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-42714172014-12-20 Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells Wang, Fang Long, Qi Gong, Yu Hu, Longbo Zhang, Hong Oettgen, Peter Peng, Tao Cell Biosci Research 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. BioMed Central 2014-12-08 /pmc/articles/PMC4271417/ /pubmed/25530841 http://dx.doi.org/10.1186/2045-3701-4-76 Text en © Wang et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Wang, Fang
Long, Qi
Gong, Yu
Hu, Longbo
Zhang, Hong
Oettgen, Peter
Peng, Tao
Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
title Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
title_full Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
title_fullStr Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
title_full_unstemmed Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
title_short Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells
title_sort epithelium-specific ets (ese)-1 upregulated gp73 expression in hepatocellular carcinoma cells
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271417/
https://www.ncbi.nlm.nih.gov/pubmed/25530841
http://dx.doi.org/10.1186/2045-3701-4-76
work_keys_str_mv AT wangfang epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells
AT longqi epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells
AT gongyu epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells
AT hulongbo epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells
AT zhanghong epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells
AT oettgenpeter epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells
AT pengtao epitheliumspecificetsese1upregulatedgp73expressioninhepatocellularcarcinomacells