ArticleCell & bioscience2014
Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells.
Article in Cell & bioscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Bridging the gap: The GOLM1-OPN-ABCG5 axis in MASH and gallstone disease: Editorial on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in metabolic dysfunction-associated steatohepatitis livers.Clinical and molecular hepatology · 2025Article
- AGR2: The Covert Driver and New Dawn of Hepatobiliary and Pancreatic Cancer Treatment.Biomolecules · 2024Review
- Golgi Phosphoprotein 73: The Driver of Epithelial-Mesenchymal Transition in Cancer.Frontiers in oncology · 2021Review
- Golgi protein 73, hepatocellular carcinoma and other types of cancers.Liver research (Beijing, China) · 2020Article
- The E-Twenty-Six Family in Hepatocellular Carcinoma: Moving into the Spotlight.Frontiers in oncology · 2020Review
- Golgi protein 73 and its diagnostic value in liver diseases.Cell proliferation · 2019Review
- Serum GP73 - An Additional Biochemical Marker for Liver Inflammation in Chronic HBV Infected Patients with Normal or Slightly Raised ALT.Scientific reports · 2019Article
- GOLPH2, a gene downstream of ras signaling, promotes the progression of pancreatic ductal adenocarcinoma.Molecular medicine reports · 2018Article
- Abnormal Expression of Golgi Protein 73 in Clinical Values and Their Role in HBV-Related Hepatocellular Carcinoma Diagnosis and Prognosis.Hepatitis monthly · 2015Article
- Screening for hepatocellular carcinoma and cholangiocarcinoma: Can biomarkers replace imaging?Current hepatology reports · 2015Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGolgi 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.
resultsThis 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.
conclusionsOur 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.
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