Hepatitis B Virus-Encoded HBsAg Contributes to Hepatocarcinogenesis by Inducing the Oncogenic Long Noncoding RNA LINC00665 through the NF-κB Pathway

Ahluwalia, Shivaksh; Ahmad, Belal; Salim, Uzma; Ghosh, Dipannita; Kamuju, Vinay; Ghosh, Arpita; Dabeer, Khadija; Menon, Manoj B.; Perumal, Vivekanandan

doi:10.1128/spectrum.02731-21

Cited by 5 publications

(3 citation statements)

References 77 publications

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“…To study the HBV replication cycle, 2.1-and 2.4-kb mRNAs were transcribed from covalently closed circular (ccc) HBV DNA from HepG2.2.15 and NTCP-G2 cells. [34][35][36] A fluorescent probe qPCR kit (Supbio Biotechnology, Guangzhou, China) was used to quantify cellular HBV cccDNA. DNA was extracted using a DNeasy Blood & Tissue Kit (Qiagen, Hilden, Germany) according to the manufacturer's instructions and denatured at 85°C for 5 min.…”

Section: Quantification Of Covalently Closed Circular Hbv Dnamentioning

confidence: 99%

“…To study the HBV replication cycle, 2.1 and 2.4 kb mRNAs were transcribed from HBV cccDNA. [34][35][36] We analyzed the expression levels of cccDNA in HepG2.2.15 and HepG2-NTCP cells to determine whether the dopamine-mediated downregulation of HBsAg and HBeAg expression was caused by an inhibition of cccDNA formation or transcription. We found that cccDNA formation was unaffected by dopamine when compared to DMSO (Fig.…”

Section: Dopamine Decreased Hbv Hbsag and Hbeag Levels But Not Cccdna...mentioning

confidence: 99%

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Dopamine Inhibits the Expression of Hepatitis B Virus Surface and e Antigens by Activating the JAK/STAT Pathway and Upregulating Interferon-stimulated Gene 15 Expression

Liu,

Pang,

Wan

et al. 2024

J Clin Transl Hepatol

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Background and Aims Hepatitis B virus (HBV) infection is a major risk factor for cirrhosis and liver cancer, and its treatment continues to be difficult. We previously demonstrated that a dopamine analog inhibited the packaging of pregenomic RNA into capsids. The present study aimed to determine the effect of dopamine on the expressions of hepatitis B virus surface and e antigens (HBsAg and HBeAg, respectively) and to elucidate the underlying mechanism. Methods We used dopamine-treated HBV-infected HepG2.2.15 and NTCP-G2 cells to monitor HBsAg and HBeAg expression levels. We analyzed interferon-stimulated gene 15 (ISG15) expression in dopamine-treated cells. We knocked down ISG15 and then monitored HBsAg and HBeAg expression levels. We analyzed the expression of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway factors in dopamine-treated cells. We used dopamine hydrochloride-treated adeno-associated virus/HBV-infected mouse model to evaluate HBV DNA, HBsAg, and HBeAg expression. HBV virus was collected from HepAD38.7 cell culture medium. Results Dopamine inhibited HBsAg and HBeAg expression and upregulated ISG15 expression in HepG2.2.15 and HepG2-NTCP cell lines. ISG15 knockdown increased HBsAg and HBeAg expression in HepG2.2.15 cells. Dopamine-treated cells activated the JAK/STAT pathway, which upregulated ISG15 expression. In the adeno-associated virus-HBV murine infection model, dopamine downregulated HBsAg and HBeAg expression and activated the JAK-STAT/ISG15 axis. Conclusions Dopamine inhibits the expression of HBsAg and HBeAg by activating the JAK/STAT pathway and upregulating ISG15 expression.

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Section: Quantification Of Covalently Closed Circular Hbv Dnamentioning

confidence: 99%

Section: Dopamine Decreased Hbv Hbsag and Hbeag Levels But Not Cccdna...mentioning

confidence: 99%

Dopamine Inhibits the Expression of Hepatitis B Virus Surface and e Antigens by Activating the JAK/STAT Pathway and Upregulating Interferon-stimulated Gene 15 Expression

Liu,

Pang,

Wan

et al. 2024

J Clin Transl Hepatol

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“…Ahluwalia et al discovered LINC00665 earlier this year to act as a mechanistic tool for HBsAg to induce hepatocarcinogenesis. By stimulating the NF-κB pathway, HBsAg induces LINC00665 levels in hepatocytes, revealing a unique method by which HBV may cause HCC (Ahluwalia et al, 2022).…”

Section: Lncrnas Involved In Hcc Diagnosis and Prognosismentioning

confidence: 99%

Decoding hepatocarcinogenesis from a noncoding RNAs perspective

El-Aziz

Dawoud

Kiriacos

et al. 2023

Journal Cellular Physiology

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Being a leading lethal malignancy worldwide, the pathophysiology of hepatocellular carcinoma (HCC) has gained a lot of interest. Yet, underlying mechanistic basis of the liver tumorigenesis is poorly understood. The role of some coding genes and their respective translated proteins, then later on, some noncoding RNAs (ncRNAs) such as microRNAs have been extensively studied in context of HCC pathophysiology; however, the implication of long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) in HCC is indeed less investigated. As a subclass of the ncRNAs which has been elusive for long time ago, lncRNAs was found to be involved in plentiful cellular functions such as DNA, RNA, and proteins regulation. Hence, it is undisputed that lncRNAs dysregulation profoundly contributes to HCC via diverse etiologies. Accordingly, lncRNAs represent a hot research topic that requires prime focus in HCC. In this review, the authors discuss breakthrough discoveries involving lncRNAs and circRNAs dysregulation that have contributed to the contemporary concepts of HCC pathophysiology and how these concepts could be leveraged as potential novel diagnostic and prognostic HCC biomarkers. Further, this review article sheds light on future trends, thereby discussing the pathological roles of lncRNAs and circRNAs in HCC proliferation, migration, and epithelial‐to‐mesenchymal transition. Along this line of reasoning, future recommendations of how these targets could be exploited to achieve effective HCC‐related drug development is highlighted.

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Multifaceted role of NF-κB in hepatocellular carcinoma therapy: Molecular landscape, therapeutic compounds and nanomaterial approaches

Guptan

Kadhim

Jalil

et al. 2023

Environmental Research

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Hepatitis B Virus-Encoded HBsAg Contributes to Hepatocarcinogenesis by Inducing the Oncogenic Long Noncoding RNA LINC00665 through the NF-κB Pathway

Abstract: Hepatitis B virus (HBV) is a major risk factor for hepatocellular carcinoma (HCC). Numerous reports indicate an oncogenic role for HBV-encoded HBsAg; however, the underlying mechanisms are not well understood.

Cited by 5 publications

References 77 publications

Dopamine Inhibits the Expression of Hepatitis B Virus Surface and e Antigens by Activating the JAK/STAT Pathway and Upregulating Interferon-stimulated Gene 15 Expression

Dopamine Inhibits the Expression of Hepatitis B Virus Surface and e Antigens by Activating the JAK/STAT Pathway and Upregulating Interferon-stimulated Gene 15 Expression

Decoding hepatocarcinogenesis from a noncoding RNAs perspective

Multifaceted role of NF-κB in hepatocellular carcinoma therapy: Molecular landscape, therapeutic compounds and nanomaterial approaches

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