ArticleJournal of translational medicine2024
PTEN deficiency potentiates HBV-associated liver cancer development through augmented GP73/GOLM1.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Hepatitis B virus promotes hepatocellular carcinoma progression by disrupting NSUN2/YBX1-mediated mVirologica Sinica · 2026Article
- TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway.Translational cancer research · 2026Article
- A label-free electrochemical aptasensor utilizing NRGO-Fc-Pt@Pd NPs for ultrasensitive detection of Golgi protein 73 in human serum.Mikrochimica acta · 2025Article
- HBV infection upregulates GP73 expression to promote liver fibrosis by enhancing ER stress via the Smad2 pathway.Immunologic research · 2025Article
- The causal relationship between hepatitis B, immunophenotypes and liver cancer: a Mendelian randomization study.Discover oncology · 2025Article
- Biomarkers for diagnosis and therapeutic options in hepatocellular carcinoma.Molecular cancer · 2024Review
- Article
- Golgi protein 73: the driver of inflammation in the immune and tumor microenvironment.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundAlthough hepatitis B virus (HBV) infection is a major risk factor for hepatic cancer, the majority of HBV carriers do not develop this lethal disease. Additional molecular alterations are thus implicated in the process of liver tumorigenesis. Since phosphatase and tensin homolog (PTEN) is decreased in approximately half of liver cancers, we investigated the significance of PTEN deficiency in HBV-related hepatocarcinogenesis.
methodsHBV-positive human liver cancer tissues were checked for PTEN expression. Transgenic HBV, Alb-Cre and Pten
resultsPten deletion and HBV transgene synergistically aggravated liver injury, inflammation, fibrosis and development of mixed hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). GP73 was augmented in HBV; Pten
conclusionsThis mixed HCC-ICC mouse model mimics liver cancer patients harboring HBV infection and PTEN/AKT signaling pathway alteration. Targeting GP73 is a promising therapeutic strategy for cancer patients with HBV infection and PTEN alteration.
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