HBV Facilitated Hepatocellular Carcinoma Cells Proliferation by Up-Regulating Angiogenin Expression Through IL-6

Zhou, Xiaotang; Yang, Fan; Yang, Ying; Hu, Ying; Liu, Weixia; Huang, ChunHong; Li, Shuping; Chen, Zhi

doi:10.1159/000488614

Cited by 14 publications

(16 citation statements)

References 41 publications

(46 reference statements)

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“…This approach mirrors other studies in which HepG2.2.15 has been compared with HepG2. 14 − 21 Nevertheless, the lack of a control vector and Geneticin within HepG2 cannot be excluded as a cause of differential results when comparing HepG2.2.15 cells against HepG2. Readers should also note that all differential proteomic results, unless otherwise noted, were acquired at 24 h post-treatment; longer or shorter treatment periods could result in significantly different profiles.…”

Section: Resultsmentioning

confidence: 99%

Deep Proteomic Deconvolution of Interferons and HBV Transfection Effects on a Hepatoblastoma Cell Line

et al. 2020

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Interferons are commonly utilized in the treatment of chronic hepatitis B virus (HBV) infection but are not effective for all patients. A deep understanding of the limitations of interferon treatment requires delineation of its activity at multiple “omic” levels. While myriad studies have characterized the transcriptomic effects of interferon treatment, surprisingly, few have examined interferon-induced effects at the proteomic level. To remedy this paucity, we stimulated HepG2 cells with both IFN-α and IFN-λ and performed proteomic analysis versus unstimulated cells. Alongside, we examined the effects of HBV transfection in the same cell line, reasoning that parallel IFN and HBV analysis might allow determination of cases where HBV transfection counters the effects of interferons. More than 6000 proteins were identified, with multiple replicates allowing for differential expression analysis at high confidence. Drawing on a compendium of transcriptomic data, as well as proteomic half-life data, we suggest means by which transcriptomic results diverge from our proteomic results. We also invoke a recent multiomic study of HBV-related hepatocarcinoma (HCC), showing that despite HBV’s role in initiating HCC, the regulated proteomic landscapes of HBV transfection and HCC do not strongly align. Special focus is applied to the proteasome, with numerous components divergently altered under IFN and HBV-transfection conditions. We also examine alterations of other protein groups relevant to HLA complex peptide display, unveiling intriguing alterations in a number of ubiquitin ligases. Finally, we invoke genome-scale metabolic modeling to predict relevant alterations to the metabolic landscape under experimental conditions. Our data should be useful as a resource for interferon and HBV researchers.

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Section: Resultsmentioning

confidence: 99%

Deep Proteomic Deconvolution of Interferons and HBV Transfection Effects on a Hepatoblastoma Cell Line

et al. 2020

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“…High expression of HMGB2 could promote the proliferation and inhibit the apoptosis of HCC cells, as well as predicting poor prognosis [23]. Researchers have demonstrated that NCAPG is associated with the growth of hepatoma cells, apoptosis, and epithelial mesenchymal transformation (EMT) [24]; NAP1L1 was found to be a nucleosome assembly protein in response to nucleosome remodelling through CSB protein and chromatin remodelling [25], promoting tumour progression as a chromatin regulatory factor in liver cancer [26]; PEA15, an essential prognostic marker for HCC, is involved in negative regulation of apoptosis signalling pathway mediated by death receptor, thereby inhibiting apoptosis of hepatoma cells. In addition, PEA15 also participates in transmembrane receptor protein tyrosine kinase signalling pathway, which mediates cell communication and promotes the migration of liver cancer cells, and the high level of ENAH expression promotes the occurrence and metastasis of liver cancer [27][28][29].…”

Section: Discussionmentioning

confidence: 99%

“…We found that TUG1 target genes NCAPG, VGLL4, HMGN4, PIGC, MCM6, NAP1L1, PEA15, GLS, HMGB2, PEA15, and ENAH were positively correlated with tumour stages (p < 0.05), suggesting that these target genes not only play a role in the development of liver cancer but also participate in tumour progression. For example, MCM6, PEA15, RACGAP1, and ENAH have been reported to promote the metastasis of HCC [17,[20][21][22][23][24][25][26][27][28][29][30]. The diagnostic effect analysis shows that TUG1 and its target genes have higher diagnostic efficacy than the traditional marker AFP in clinics, so further clinical trials are needed.…”

Section: Discussionmentioning

confidence: 99%

The identification and preliminary study of lncRNA TUG1 and its related genes in hepatocellular carcinoma

Liu

Peng

et al. 2019

Arch Med Sci

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Introduction: Hepatocellular carcinoma (HCC) is a common malignant tumour of the digestive system, which is a threat to public health. The purpose of this study was to investigate the featured genes and pathways of HCC from a bioinformatics database, and verify their correlation with diagnosis and prognosis of HCC. Material and methods: We downloaded the gene expression profile on HCC from the Gene Expression Omnibus (GEO), and software R was used to identify differentially expressed lncRNA (DEL). The target genes of the lncRNA were further predicted by using a cluster database and molecular interaction database. Subsequently, a combined interaction network of target genes was constructed using the Cytoscape platform with preliminary verification at the level of different databases, cell lines, and tissues. Finally, we explored the effectiveness of TUG1 and its target genes on the diagnosis and prognosis of HCC by univariate Cox analysis and survival analysis. Results: A total of four DELs were identified and the most remarkably up-regulated lncRNA was TUG1, which included 12 high-confidence target genes. Moreover, we found that the expression changes of TUG1 and its target genes in different databases, cell lines, and liver cancer tissues were consistent with the prediction. The high expression of TUG1 and its target genes could significantly predict the shorter survival time of HCC patients, among which NCAPG, MCM6, PIGC, PEA15, and RACGAP1 have significant diagnostic value for HCC (AUC > 0.9). Conclusions: This study provides a starting point for the screening of therapeutically relevant targets in HCC. Further experiment should be conducted to verify our findings.

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“…Excessive secretion of SASP components has also been reported in chronic hepatitis B, while HBV infection has been associated with elevated levels of angiogenin‐2. In particular, transfection of HepG2.2.15 cells or HepG2 cells with HBx plasmid was shown to lead to increased secretion of interleukin‐6 (IL‐6) which resulted in increased expression of angiogenin‐2 32 …”

Section: Interplay Between Hbv and Cellular Senescencementioning

confidence: 99%

Cellular senescence and hepatitis B‐related hepatocellular carcinoma: An intriguing link

Karakousis

Papatheodoridi

Chatzigeorgiou

et al. 2020

Liver International

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Chronic hepatitis B is mainly responsible for the morbidity and mortality from hepatitis B virus (HBV)‐related complications, including hepatocellular carcinoma (HCC) and decompensated cirrhosis. Hepatocellular carcinoma remains the main challenge in the management of not only undiagnosed and/or untreated but also diagnosed and treated patients with chronic HBV infection, as its incidence decreases but is not eliminated even after many years of effective anti‐HBV therapy. The exact mechanisms used by HBV to cause malignant transformation remain uncertain, although much of the available data are in favour of a pathogenetic role of HBx protein. Senescence is a cellular state, in which cells lose their ability to proliferate. This biological mechanism may function in a dual mode, namely being both cancer‐protective as a result of reduced cellular proliferation, but also cancer‐enhancing as a result of modulation of the tissular microenvironment by immune cells during persistent accumulation of senescent cells. Protein X of HBV protein exhibits many similarities in terms of the implemented mechanisms of action and pathways related to the biological process of cellular senescence. Concurrently, insufficient clearance of both senescent and precancerous hepatocytes combined with inadequate immune surveillance as a result of immunosenescence caused by chronic HBV infection may lead to hepatocarcinogenesis. Thus, the effect of HBV seems to be critical as a connecting link between cellular senescence and development of HCC. An ongoing research is underway towards identifying and validating markers of hepatocyte senescence, which could improve the landscape for evaluation of chronic liver disease, thereby providing valuable information in terms of HBV‐related carcinogenesis.

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HBV Facilitated Hepatocellular Carcinoma Cells Proliferation by Up-Regulating Angiogenin Expression Through IL-6

Cited by 14 publications

References 41 publications

Deep Proteomic Deconvolution of Interferons and HBV Transfection Effects on a Hepatoblastoma Cell Line

Deep Proteomic Deconvolution of Interferons and HBV Transfection Effects on a Hepatoblastoma Cell Line

The identification and preliminary study of lncRNA TUG1 and its related genes in hepatocellular carcinoma

Cellular senescence and hepatitis B‐related hepatocellular carcinoma: An intriguing link

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