ArticleScientific reports2016
USP16 Downregulation by Carboxyl-terminal Truncated HBx Promotes the Growth of Hepatocellular Carcinoma Cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 68 citations in OpenAlex.
- Hepatitis B virus integration and hepatocarcinogenesis.Liver research (Beijing, China) · 2025Review
- Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025Review
- Drug resistance mechanisms and treatment strategies mediated by Ubiquitin-Specific Proteases (USPs) in cancers: new directions and therapeutic options.Molecular cancer · 2024Review
- Role of Ubiquitin-specific Proteases in Hepatocellular Carcinoma Pathogenesis.Current topics in medicinal chemistry · 2024Review
- Review
- Critical role of lncEPAT in coupling dysregulated EGFR pathway and histone H2A deubiquitination during glioblastoma tumorigenesis.Science advances · 2022Article
- Hepatitis B virus X protein mediated epigenetic alterations in the pathogenesis of hepatocellular carcinoma.Hepatology international · 2022Review
- Research Progress of DUB Enzyme in Hepatocellular Carcinoma.Frontiers in oncology · 2022Review
- MYSM1 inhibits human colorectal cancer tumorigenesis by activating miR-200 family members/CDH1 and blocking PI3K/AKT signaling.Journal of experimental & clinical cancer research : CR · 2021Article
- LINC01348 suppresses hepatocellular carcinoma metastasis through inhibition of SF3B3-mediated EZH2 pre-mRNA splicing.Oncogene · 2021Article
- Article
- CRISPR-Cas9 Editing of Human Histone Deubiquitinase GeneFrontiers in cell and developmental biology · 2021Article
- Substrate-specific recognition of IKKs mediated by USP16 facilitates autoimmune inflammation.Science advances · 2021Article
- Knockdown of ubiquitin-specific peptidase 13 inhibits cell growth of hepatocellular carcinoma by reducing c-Myc expression.The Kaohsiung journal of medical sciences · 2020Article
- USP16 counteracts mono-ubiquitination of RPS27a and promotes maturation of the 40S ribosomal subunit.eLife · 2020Article
- miR-613 Suppresses Chemoresistance and Stemness in Triple-Negative Breast Cancer by Targeting FAM83A.Cancer management and research · 2020Article
- The multiple roles of deubiquitinases in liver cancer.American journal of cancer research · 2020Review
- Transcriptional activation of USP16 gene expression by NFκB signaling.Molecular brain · 2019Article
- Development of a DUB-selective fluorogenic substrate.Chemical science · 2019Article
- Deubiquitinating Enzymes: A Critical Regulator of Mitosis.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) infection is a major factor that contributes to the development of hepatocellular carcinoma (HCC). HBV X protein (HBx) has been shown to accelerate HCC progression by promoting tumour growth and metastasis. In the clinic, carboxyl-terminal truncated HBx (Ct-HBx) proteins are frequently present in HCC tumour tissues, but not in non-tumorous tissues. In this study, we analysed deubiquitinase expression profiles in cells with or without ectopic expression of the Ct-HBx proteins and observed that the expression of ubiquitin specific peptidase 16 (USP16) was substantially inhibited by Ct-HBx proteins. Liver tumour cells with forced down-regulation of USP16 exhibited increased capabilities for colony formation and tumour growth in vivo. In addition, USP16 inhibition promoted stem-like properties in tumour cells, as evidenced by their spheroid formation and chemo-responsiveness. Furthermore, ectopic expression of USP16 in tumour cells significantly abrogated the tumour promoting activities of the Ct-HBx proteins (HBxΔ35), leading to decreased tumour cell viability and tumour growth. In human HCCs, USP16 was frequently downregulated, and the decreased expression of USP16 was correlated with high tumour stages and poor differentiation status. Taken together, our study suggests that USP16 downregulation is a critical event in Ct-HBx-mediated promotion of HCC tumorigenicity and malignancy.
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