ArticleInternational journal of molecular sciences2013
CXCL10 decreases GP73 expression in hepatoma cells at the early stage of hepatitis C virus (HCV) infection.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Dual role of CXCL10 in cancer progression: implications for immunotherapy and targeted treatment.Cancer biology & therapy · 2025Review
- Deficiency of ASGR1 promotes liver injury by increasing GP73-mediated hepatic endoplasmic reticulum stress.Nature communications · 2024Article
- Golgi protein 73: the driver of inflammation in the immune and tumor microenvironment.Frontiers in immunology · 2024Review
- Integrating Single-Cell and Spatial Transcriptomics to Uncover and Elucidate GP73-Mediated Pro-Angiogenic Regulatory Networks in Hepatocellular Carcinoma.Research (Washington, D.C.) · 2024Article
- The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021Review
- Golgi protein 73 and its diagnostic value in liver diseases.Cell proliferation · 2019Review
- A Nonsynonymous Variant in the GOLM1 Gene in Cutaneous Malignant Melanoma.Journal of the National Cancer Institute · 2018Article
- Abnormal Expression of Golgi Protein 73 in Clinical Values and Their Role in HBV-Related Hepatocellular Carcinoma Diagnosis and Prognosis.Hepatitis monthly · 2015Article
- LRRFIP1 Inhibits Hepatitis C Virus Replication by Inducing Type I Interferon in Hepatocytes.Hepatitis monthly · 2015Article
- Effect of GP73 silencing on proliferation and apoptosis in hepatocellular cancer.World journal of gastroenterology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Golgi protein 73 (GP73), which is up-regulated in hepatocellular carcinoma (HCC), has recently been identified as a novel serum marker for HCC diagnosis. Several reports also noted the increased levels of GP73 expression in chronic liver disease in patients with acute hepatitis of various etiologies, chronic Hepatitis C virus (HCV) infection and alcoholic liver disease. The molecular mechanisms of GP73 expression in HCV related liver disease still need to be determined. In this study, we aimed to evaluate the effect of HCV infection on GP73 expression. GP73 was highly expressed in Huh7, Hep3B, 293T and HUVEC cells, and was low-expressed in HepG2 cells. HCV infection led to down-regulation of GP73 in Huh7 and HepG2/CD81 cells at the early stage of infection. CXCL10 decreased GP73 expression in Huh7 and HepG2 cells. Up-regulation of GP73 was noted in hepatocytes with cytopathic effect at advanced stage of HCV infection, and further research is needed to determine the unknown factors affecting GP73 expression. In conclusion, our study provided additional evidence for the roles of GP73 in liver disease.
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