ArticleVirologica Sinica2023
HBV precore G1896A mutation promotes growth of hepatocellular carcinoma cells by activating ERK/MAPK pathway.
Article in Virologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- Precore mutation enhances viral replication to facilitate persistent infection especially in HBeAg-negative patients.Virologica Sinica · 2024Pooled it
- The load of hepatitis B virus reduces the immune checkpoint inhibitors efficiency in hepatocellular carcinoma patients.Frontiers in immunology · 2024Pooled it
- Cholesterol metabolism dysregulated by key HBV mutations revealed through multi-omics profiling.iScience · 2026Article
- HBV reprograms the tumor microenvironment in hepatocellular carcinoma: mechanisms and therapeutic implications.Clinical and experimental medicine · 2026Review
- Review
- Molecular Network Analysis of HBV Persistent Infection from the Perspective of Whole Transcriptome.Biomolecules · 2025Article
- Personalized prognosis in unresectable hepatocellular carcinoma: Development and validation of a model for transcatheter arterial chemoembolization plus lenvatinib.World journal of gastrointestinal oncology · 2025Article
- Article
- Article
- The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways.Frontiers in microbiology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection is one of the leading causes of hepatocellular carcinoma (HCC). The HBV genome is prone to mutate and several variants are closely related to the malignant transformation of liver disease. G1896A mutation (G to A mutation at nucleotide 1896) is one of the most frequently observed mutations in the precore region of HBV, which prevents HBeAg expression and is strongly associated with HCC. However, the mechanisms by which this mutation causes HCC are unclear. Here, we explored the function and molecular mechanisms of the G1896A mutation during HBV-associated HCC. G1896A mutation remarkably enhanced the HBV replication in vitro. Moreover, it increased tumor formation and inhibited apoptosis of hepatoma cells, and decreased the sensitivity of HCC to sorafenib. Mechanistically, the G1896A mutation could activate ERK/MAPK pathway to enhanced sorafenib resistance in HCC cells and augmented cell survival and growth. Collectively, our study demonstrates for the first time that the G1896A mutation has a dual regulatory role in exacerbating HCC severity and sheds some light on the treatment of G1896A mutation-associated HCC patients.
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Registered trials
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.