ArticleJournal of cellular biochemistry2018
CRISPR/Cas9-mediated knockout of HBsAg inhibits proliferation and tumorigenicity of HBV-positive hepatocellular carcinoma cells.
Article in Journal of cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 53 citations in OpenAlex.
- Virus infections and cancers: from mechanisms to therapeutics.Molecular biomedicine · 2026Review
- Targeting ferroptosis induction via nanomaterials in hepatocellular carcinoma: an insight into mechanism and therapeutic potential.Journal of nanobiotechnology · 2026Review
- Functional cure for chronic hepatitis B on hepatocellular carcinoma prevention: Evidence and clinical implications.iLIVER · 2026Review
- The APOBEC3 family: a narrative review of an alternative therapeutic agent for hepatitis B virus-induced hepatocellular carcinoma.Journal of gastrointestinal oncology · 2026Review
- BIRC5 as a master regulator in HCC: unraveling its role in tumor survival and therapeutic potential.Functional & integrative genomics · 2025Article
- CRISPR/Cas9 system: a novel approach to overcome chemotherapy and radiotherapy resistance in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Mechanisms of hepatocellular carcinoma and cirrhosis development in concurrent steatotic liver disease and chronic hepatitis B.Clinical and molecular hepatology · 2025Review
- Relationship between HBsAg/HBV DNA and prognosis in patients with HBV-related hepatocellular carcinoma treated with PD-1/PD-L1 inhibitors.Therapeutic advances in medical oncology · 2025Article
- Association of IL-6 G-174C (rs1800795) variant with the susceptibility to hepatocellular carcinoma in patients with chronic hepatitis.Journal of the Egyptian National Cancer Institute · 2024Article
- Harnessing CRISPR technology for viral therapeutics and vaccines: from preclinical studies to clinical applications.Virus research · 2024Review
- A review of the literature on the use of CRISPR/Cas9 gene therapy to treat hepatocellular carcinoma.Oncology research · 2024Review
- CRISPR/Cas9 as a New Antiviral Strategy for Treating Hepatitis Viral Infections.International journal of molecular sciences · 2023Review
- Multi-faceted CRISPR/Cas technological innovation aspects in the framework of 3P medicine.The EPMA journal · 2023Review
- CRISPR/Cas9 for hepatitis B virus infection treatment.Immunity, inflammation and disease · 2023Review
- Advances in CRISPR therapeutics.Nature reviews. Nephrology · 2023Review
- Gene Editing Technologies to Target HBV cccDNA.Viruses · 2022Review
- The power and the promise of CRISPR/Cas9 genome editing for clinical application with gene therapy.Journal of advanced research · 2022Review
- CRISPR/Cas9 application in cancer therapy: a pioneering genome editing tool.Cellular & molecular biology letters · 2022Review
- Viral hepatitis: Past, present, and future.World journal of gastroenterology · 2022Review
- Therapeutic potentials of CRISPR-Cas genome editing technology in human viral infections.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection remains the most common risk factor for hepatocellular carcinoma (HCC). High HBV surface antigen (HBsAg) levels are highly correlated with hepatocarcinogenesis and HBV-associated HCC development. However, the role and detailed mechanisms associated with HBsAg in HCC development remain elusive. In this study, we designed specific single guide RNAs (sgRNAs) targeting the open reading frames, preS1/preS2/S, of the HBV genome and established HBsAg knockout HCC cell lines using the CRISPR/Cas9 system. We showed that knockout of HBsAg in HCC cell lines decreased HBsAg expression and significantly attenuated HCC proliferation in vitro, as well as tumorigenicity in vivo. We also found that overexpression of HBsAg, including the large (LHBs), middle (MHBs), and small (SHBs) surface proteins promoted proliferation and tumor formation in HCC cells. Moreover, we demonstrated that knockout of HBsAg in HCC cells decreased interleukin (IL)-6 production and inhibited signal transducer and activator of transcription 3 (STAT3) signaling, while overexpression of HBsAg induced a substantial accumulation of pY-STAT3. Collectively, these results highlighted the tumorigenic role of HBsAg and implied that the IL-6-STAT3 pathway may be implicated in the HBsAg-mediated malignant potential of HBV-associated HCC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.