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Human liver organoids a patient-derived primary model for HBV Infection, Replication and Related Hepatocellular Carcinoma

ABSTRACT: Human liver organoids a patient-derived primary model for HBV Infection, Replication and Related Hepatocellular Carcinoma

PROVIDER: PRJNA523341 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15074079.fastq.gz	Fastqsanger.gz
	SRR15074080.fastq.gz	Fastqsanger.gz
	SRR15074081.fastq.gz	Fastqsanger.gz
	SRR15074082.fastq.gz	Fastqsanger.gz
	SRR15074083.fastq.gz	Fastqsanger.gz

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Human liver organoids; a patient-derived primary model for HBV Infection, Replication and Related Hepatocellular Carcinoma

Project description:Here we interrogate the potential of human liver organoids as a platform for modeling HBV infection and related tumorigenesis. We show that organoids derived from HBV-infected patients display an aberrant early cancer gene signature, which clusters with the HCC cohort on the TCGA LIHC dataset and away from healthy liver tissue.

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Comprehensive analysis of the miRNA profile between HBV-related Hepatocellular carcinoma (HBCC) and no HBV-related Hepatocellular carcinoma (HNCC)

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Comprehensive analysis of the mRNA-lncRNA profile between HBV-related Hepatocellular carcinoma (HBCC) and no HBV-related Hepatocellular carcinoma (HNCC)

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NEDD4-binding protein 1 suppresses HBV replication by regulating HBV RNAs

Project description:Background and Aims Chronic infection with hepatitis B virus (HBV) has been known to cause liver cirrhosis and hepatocellular carcinoma. Although nucleos(t)ide analogs are mainly used for the treatment of HBV, they require long-term administration and may lead to the emergence of drug resistance. Therefore, to identify targets for the development of novel anti-HBV therapies, we screened HBV-suppressive host factors using RNA-bnding protein (RBP) expression plasmids library. Approach and Results We screened the RBP library by generating overexpressing RBP cell lines and observing anti-HBV effect. As a result, we identified NEDD4-binding protein 1 (N4BP1) as a candidate showing anti-HBV effect. In hepatocellular carcinoma cell lines, overexpression of N4BP1 decreased the relaxed circular DNA (rcDNA) levels, while suppression of N4BP1 expression increased rcDNA levels. Restoring N4BP1 expression in N4BP1 knockout cells regained the anti-HBV effect of N4BP1. Next, we constructed KH-like and RNase domain-deficient mutants of N4BP1 and examined their effects on HBV replication, and found that both the KH-like and RNase domains are required for its anti-HBV effect. N4BP1 suppresses the step where pregenomic RNA (pgRNA) is synthesized in the HBV life cycle by promoting degradation of pgRNA. Transcriptome analyses of primary human hepatocytes overexpressing N4BP1 suggested that N4BP1 may have anti-HBV activity independent of other host factors. Conclusions In summary, N4BP1 was found to be a novel anti-HBV factor. N4BP1 inhibited HBV replication by promoting pgRNA degradation.

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SENP3-mediated host defense response contains HBV replication and restores protein synthesis

Project description:Certain organs are capable of containing the replication of various types of viruses. In the liver, infection of Hepatitis B virus (HBV), the etiological factor of Hepatitis B and hepatocellular carcinoma (HCC), often remains asymptomatic and leads to a chronic carrier state. Here we investigated how hepatocytes contain HBV replication and promote their own survival by orchestrating a translational defense mechanism via the stress-sensitive SUMO-2/3-specific peptidase SENP3. We found that SENP3 expression level decreased in HBV-infected hepatocytes in various models including HepG2-NTCP cell lines and a humanized mouse model. Downregulation of SENP3 reduced HBV replication and boosted host protein translation. We also discovered that IQGAP2, a Ras GTPase-activating-like protein, is a key substrate for SENP3-mediated de-SUMOylation. Downregulation of SENP3 in HBV infected cells facilitated IQGAP2 SUMOylation and degradation, which leads to suppression of HBV gene expression and restoration of global translation of host genes via modulation of AKT phosphorylation. Thus, The SENP3-IQGAP2 de-SUMOylation axis is a host defense mechanism of hepatocytes that restores host protein translation and suppresses HBV gene expression.

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Sera of individuals chronically infected with hepatitis B virus (HBV) contain diverse RNA types produced by HBV replication or derived from integrated HBV DNA

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2023-02-26 | GSE224901 | GEO

Comprehensive analysis of the miRNA profile between HBV-related Hepatocellular carcinoma (HBCC) and no HBV-related Hepatocellular carcinoma (HNCC)

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Transgelin modulates HBV replication and transcription via OPA1-mediated mitochondrial dynamics

Project description:Hepatitis B virus (HBV) hijacks host proteins to manipulate cellular physiology and metabolism, facilitating its replication. Transgelin 2 (TAGLN2) ，an actin-binding protein, is highly expressed in HBV-associated hepatocellular carcinoma, yet its role in viral infection remains unclear. I Here, we demonstrated that HBV upregulated TAGLN expression in vitro and in vivo. TAGLN depletion impaired HBV replication and transcription while promoted mitochondrial fission and enhanced ATP production. Through mitochondrial proteomics, we identified Optic Atrophy 1 (OPA1)，a key dynamin governing mitochondrial fusion, as a downstream effector. Silencing OPA1 downregulated TAGLN and suppressed HBV replication, whereas OPA1 overexpression exerted the opposite effects. Mechanistically, TAGLN and OPA1 form a reciprocal regulatory axis to sustain HBV propagation. Our study unveils a novel TAGLN-OPA1 axis critical for HBV replication, providing insights into host-directed antiviral strategies.

2025-04-15 | PXD063056 |

Comprehensive analysis of the mRNA-lncRNA profile between HBV-related Hepatocellular carcinoma (HBCC) and no HBV-related Hepatocellular carcinoma (HNCC)

Project description:Comprehensive analysis of the mRNA-lncRNA profile between HBV-related Hepatocellular carcinoma (HBCC) and no HBV-related Hepatocellular carcinoma (HNCC)

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Next Generation Sequencing Identification of HBV-MLL4 integration and its molecular basis in Chinese hepatocellular carcinoma

Project description:Purpose: To gain molecular insights of HBV integration that may contribute to HCC tumorigenesis, we performed whole transcriptome sequencing and whole genome copy number profiling of hepatocellular carcinoma (HCC) samples from 50 Chinese patients. Results: We identified a total of 33 HBV-human integration sites in 16 of 44 HBV-positive HCC tissues, which were enriched in HBV genotype C-infected patients. In addition, significantly recurrent HBV-MLL4 integration (18%). This dataset is part of the TransQST collection.

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