Hepatitis B virus X protein influences enrichment profiles of H3K9me3 on promoter regions in human hepatoma cell lines

Wang, Diyi; An, Shuhong; Liu, Lei; Bai, Shanshan; Wu, Kai-Xiang; Zhu, Rong; Wang, Zhaojin

doi:10.18632/oncotarget.12751

Cited by 9 publications

(7 citation statements)

References 33 publications

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“…1f ). Btbd17 has no known function besides epigenetic dysregulation in hepatocellular carcinoma 29 , while Grasp regulates neuronal intracellular trafficking and metabotropic glutamate receptor organization 30 . In contrast, EPlo uniquely and differentially expressed Fev and St18 , a paralog of Myt1.…”

Section: Resultsmentioning

confidence: 99%

Endocrine lineage biases arise in temporally distinct endocrine progenitors during pancreatic morphogenesis

et al. 2018

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Decoding the molecular composition of individual Ngn3 + endocrine progenitors (EPs) during pancreatic morphogenesis could provide insight into the mechanisms regulating hormonal cell fate. Here, we identify population markers and extensive cellular diversity including four EP subtypes reflecting EP maturation using high-resolution single-cell RNA-sequencing of the e14.5 and e16.5 mouse pancreas. While e14.5 and e16.5 EPs are constantly born and share select genes, these EPs are overall transcriptionally distinct concomitant with changes in the underlying epithelium. As a consequence, e16.5 EPs are not the same as e14.5 EPs: e16.5 EPs have a higher propensity to form beta cells. Analysis of e14.5 and e16.5 EP chromatin states reveals temporal shifts, with enrichment of beta cell motifs in accessible regions at later stages. Finally, we provide transcriptional maps outlining the route progenitors take as they make cell fate decisions, which can be applied to advance the in vitro generation of beta cells.

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Section: Resultsmentioning

confidence: 99%

Endocrine lineage biases arise in temporally distinct endocrine progenitors during pancreatic morphogenesis

et al. 2018

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“…HBx protein also promotes the proliferation of hepatoma cells. Wang et al found that HBx downregulated tumor-suppressor p16 gene by methylation of some CpG sites in the promoter region [44]. HBx protein activates the Wnt/β-catenin pathway which results in the acceleration of hepatoma cell proliferation [45].…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B Virus-X Downregulates Expression of Selenium Binding Protein 1

Lee

Kim

Park

et al. 2020

Viruses

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Selenium binding protein 1 (SELENBP1) has been known to be reduced in various types cancer, and epigenetic change is shown to be likely to account for the reduction of SELNEBP1 expression. With cDNA microarray comparative analysis, we found that SELENBP1 is markedly decreased in hepatitis B virus-X (HBx)-expressing cells. To clarify the effect of HBx on SELENBP1 expression, we compared the expression levels of SELENBP1 mRNA and protein by semi-quantitative RT-PCR, Northern blot, and Western blot. As expected, SELENBP1 expression was shown to be reduced in cells expressing HBx, and reporter gene analysis showed that the SELENBP1 promoter is repressed by HBx. In addition, the stepwise deletion of 5′ flanking promoter sequences resulted in a gradual decrease in basal promoter activity and inhibition of SELENBP1 expression by HBx. Moreover, immunohistochemistry on tissue microarrays containing 60 pairs of human liver tissue showed decreased intensity of SELENBP1 in tumor tissues as compared with their matched non-tumor liver tissues. Taken together, our findings suggest that inhibition of SELENBP1 expression by HBx might act as one of the causes in the development of hepatocellular carcinoma caused by HBV infection.

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“…While ZNFs are best known as DNA-binding domains, it has become clear that ZNF domains can bind with RNA, lipids, and methylated DNA, as well as proteins and PTMs such as SUMO, ubiquitin, PAR, and methylation [36] . A few ZNF proteins have been reported to be associated with viral infection [ 37 , 38 ]. Among the reports already available about ZNF205, no report is relevant to viral infection.…”

Section: Discussionmentioning

confidence: 99%

ZNF205 positively regulates RLR antiviral signaling by targeting RIG-I

Zhong,

Wang,

Weng

et al. 2023

ABBS

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Retinoic acid-inducible gene I (RIG-I) is a cytosolic viral RNA receptor. Upon viral infection, the protein recognizes and then recruits adapter protein mitochondrial antiviral signaling (MAVS) protein, initiating the production of interferons and proinflammatory cytokines to establish an antiviral state. In the present study, we identify zinc finger protein 205 (ZNF205) which associates with RIG-I and promotes the Sendai virus (SeV)-induced antiviral innate immune response. Overexpression of ZNF205 facilitates interferon-beta (IFN-β) introduction, whereas ZNF205 deficiency restricts its introduction. Mechanistically, the C-terminal zinc finger domain of ZNF205 interacts with the N-terminal tandem caspase recruitment domains (CARDs) of RIG-I; this interaction markedly promotes K63 ubiquitin-linked polyubiquitination of RIG-I, which is crucial for RIG-I activation. Thus, our results demonstrate that ZNF205 is a positive regulator of the RIG-I-mediated innate antiviral immune signaling pathway.

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Hepatitis B virus X protein influences enrichment profiles of H3K9me3 on promoter regions in human hepatoma cell lines

Cited by 9 publications

References 33 publications

Endocrine lineage biases arise in temporally distinct endocrine progenitors during pancreatic morphogenesis

Endocrine lineage biases arise in temporally distinct endocrine progenitors during pancreatic morphogenesis

Hepatitis B Virus-X Downregulates Expression of Selenium Binding Protein 1

ZNF205 positively regulates RLR antiviral signaling by targeting RIG-I

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