Novel protein kinase C phosphorylated kinase inhibitor-matrine suppresses replication of hepatitis B virus via modulating the mitogen-activated protein kinase signal

Zhou, Shen; Li, Yuan; Gao, Jing; Wang, Yanyan; Xin-ping, MA; Ding, Hui; Li, Xiuling; Sun, Suofeng

doi:10.1080/21655979.2021.2024957

Cited by 8 publications

(3 citation statements)

References 58 publications

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“…Some studies indicate that HBx does not affect PKC activity, nor that PKC is important for HBx-dependent transcriptional instigation. 22 In contrast, there is also evidence describing the dependence of HBx on PKC stimulation, which has been satisfied by an increased level of DAG in HBx-processing cells. This implies that PKC is crucial in HBx-dependent stimulation of NF-kB or AP1.…”

Section: Hepatitis B Virus (Hbv)mentioning

confidence: 99%

“…The inspection of the protein kinase C (PKC)/HBx interaction is one example of evidence that targeted the interference of HBx on the signal cascade and correlated it with the putative effect of HBx on HBV-related oncogenesis. Some studies indicate that HBx does not affect PKC activity, nor that PKC is important for HBx-dependent transcriptional instigation . In contrast, there is also evidence describing the dependence of HBx on PKC stimulation, which has been satisfied by an increased level of DAG in HBx-processing cells.…”

Section: Viruses Associated With Oncogenesismentioning

confidence: 99%

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Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities

Chowdhary,

Deka,

Panda

et al. 2023

Mol. Pharmaceutics

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Human viral oncogenesis is a complex phenomenon and a major contributor to the global cancer burden. Several recent findings revealed cellular and molecular pathways that promote the development and initiation of malignancy when viruses cause an infection. Even, antiviral treatment has become an approach to eliminate the viral infections and prevent the activation of oncogenesis. Therefore, for a better understanding, the molecular pathogenesis of various oncogenic viruses like, hepatitis virus, human immunodeficiency viral (HIV), human papillomavirus (HPV), herpes simplex virus (HSV), and Epstein-Barr virus (EBV), could be explored, especially, to expand many potent antivirals that may escalate the apoptosis of infected malignant cells while sparing normal and healthy ones. Moreover, contemporary therapies, such as engineered antibodies antiviral agents targeting signaling pathways and cell biomarkers, could inhibit viral oncogenesis. This review elaborates the recent advancements in both natural and synthetic antivirals to control viral oncogenesis. The study also highlights the challenges and future perspectives of using antivirals in viral oncogenesis.

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Section: Hepatitis B Virus (Hbv)mentioning

confidence: 99%

Section: Viruses Associated With Oncogenesismentioning

confidence: 99%

Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities

Chowdhary,

Deka,

Panda

et al. 2023

Mol. Pharmaceutics

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“…The hepatitis B virus (HBV) is still the leading cause of liver fibrosis in China [ 6 ]. More and more evidence indicates that HBV infection may promote the production of transforming growth factor- β in liver cells, which in turn activates hepatic stellate cells and accelerates liver fibrosis [ 7 , 8 ]. TGF- β is mainly produced by activated macrophages in the liver, which stimulates the activation of hepatic stellate cells (HSCs) into a myofibroblast-like phenotype [ 9 , 10 ], promotes the differentiation of myofibroblasts, and stimulates the synthesis of extracellular matrix and down-regulating the degradation of extracellular matrix [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Protein Acetylation Increased Risk of Fibrosis-Related Liver Cancer

Wang

Song³

et al. 2023

Journal of Oncology

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Objective. The occurrence of liver fibrosis and fibrosis-related liver cancer is the reason for the increase in morbidity and mortality worldwide. Transforming growth factor-β2 (TGF-β2) is an important mediator of chronic liver fibrosis. This study aims to find the molecular mechanism that mediates HBV infection and induces TGF-β2 and verifies that CREB binding protein acetylation mediates HBV infection and induces TGF-β2 expression. Methods. The acetylated proteins were extracted from HepG2-NTCP cells and HBV-infectedHepG2-NTCP cells. The acetylated proteins were screened by modification enrichment technology and database search. Protein annotation, motif analysis of modification sites, and protein function enrichment analysis of these proteins were performed to roughly clarify the location and function of these acetylated modification proteins in cells. Acylated proteins enriched in the TGF-β pathway were obtained by KEGG pathway enrichment analysis. The effect of the selected acetylated modification protein on the TGF-β pathway was verified by experiments, that is, the target protein gene was knocked out by siRNA, and the expression level of the TGF-β2 was detected by qRT-PCR. Results. Proteins were extracted from HepG2-NTCP cells and HepG2-NTCP cells infected with HBV, and differential acetylation modification proteins were screened. The target protein CREB binding protein was screened by modification enrichment technology and database search. The aggregation analysis of TGF-β pathway showed that CREB binding protein was acetylated at amino acid positions 434 and 439, and enriched in the TGF-β signaling pathway. siRNA targeting CREB binding protein was transfected, and the expression of TGF-β2 in cells was detected by qRT-PCR and western blot, respectively. It was verified that HBV infection-inducedCREB-binding protein acetylation regulated the high expression of TGF-β2. Conclusion. After HBV infection, CREBBP acetylation was up-regulated, which promoted the high expression of TGF-β2.

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SRPKIN-1 as an inhibitor against hepatitis B virus blocking the viral particle formation and the early step of the viral infection

Li,

Nakashima,

Ito

et al. 2023

Antiviral Research

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Novel protein kinase C phosphorylated kinase inhibitor-matrine suppresses replication of hepatitis B virus via modulating the mitogen-activated protein kinase signal

Cited by 8 publications

References 58 publications

Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities

Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities

Protein Acetylation Increased Risk of Fibrosis-Related Liver Cancer

SRPKIN-1 as an inhibitor against hepatitis B virus blocking the viral particle formation and the early step of the viral infection

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