From infection to cancer: how DNA tumour viruses alter host cell central carbon and lipid metabolism

Magon, Kamini L; Parish, Joanna L

doi:10.1098/rsob.210004

Cited by 11 publications

(15 citation statements)

References 90 publications

(120 reference statements)

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“…Previous studies have found that viral carcinogenesis was associated with glucose and lipid metabolism. For example, Epstein-Barr virus (EBV) is a gamma herpesvirus that is highly prevalent in the human population, which almost all adults are seropositive [ 36 ]. It was reported that the prevalence of EBV was significantly higher in diabetic patients than in the individuals without diabetes [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that the prevalence of EBV was significantly higher in diabetic patients than in the individuals without diabetes [ 37 ]. EBV has been indicated to manipulate host cell lipid metabolism in both epithelial and B cells, and it was indicated that manipulation of lipid metabolism may play a role in host cell transformation and carcinogenesis [ 36 ]. Therefore, the mRNA HIST1H2BM in the above pathways might play a role in participating in lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

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Identified lncRNAs functional modules and genes in prediabetes with hypertriglyceridemia by weighted gene co-expression network analysis

et al. 2022

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Background Hypertriglyceridemia (HTG) is one of the most important comorbidities in abnormal glucose patients. The aim of this study was to identify lncRNAs functional modules and hub genes related to triglyceride (TG) in prediabetes. Methods The study included 12 prediabetic patients: 6 participants with HTG and 6 participants with normal triglyceride (NTG). Whole peripheral blood RNA sequencing was performed for these samples to establish a lncRNA library. WGCNA, KEGG pathways analysis and the PPI network were used to construct co‐expression network, to obtain modules related to blood glucose, and to detect key lncRNAs. Meanwhile, GEO database and qRT-PCR were used to validate above key lncRNAs. Results We found out that the TCONS_00334653 and PVT1, whose target mRNA are MYC and HIST1H2BM, were downregulating in the prediabetes with HTG. Moreover, both of TCONS_00334653 and PVT1 were validated in the GEO database and qRT-PCR. Conclusions Therefore, the TCONS_00334653 and PVT1 were detected the key lncRNAs for the prediabetes with HTG, which might be a potential therapeutic or diagnostic target for the treatment of prediabetes with HTG according to the results of validation in the GEO database, qRT-PCR and ROC curves.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Identified lncRNAs functional modules and genes in prediabetes with hypertriglyceridemia by weighted gene co-expression network analysis

et al. 2022

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“…EBNA2-driven MYC expression can upregulate mitochondrial one-carbon metabolism, specifically the de novo synthesis of serine, which contributes to nucleotide synthesis, mitochondrial NADPH production and production of the antioxidant glutathione [ 88 ]. Other metabolic pathways upregulated by EBNA2-driven expression of MYC in B cells include cholesterol and lipid biosynthesis [ 89 , 90 ].…”

Section: Regulation Of Myc By Dna Tumor Virus Oncoproteinsmentioning

confidence: 99%

“…BCL2L11 expression can be induced by MYC in the absence of EBNA3A and EBNA3C in a negative feedback mechanism [93][94][95]. expression of MYC in B cells include cholesterol and lipid biosynthesis [89,90].…”

Section: Regulation Of Myc By Ebvmentioning

confidence: 99%

Metabolic Control by DNA Tumor Virus-Encoded Proteins

Prusinkiewicz

Mymryk

2021

Pathogens

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Viruses co-opt a multitude of host cell metabolic processes in order to meet the energy and substrate requirements for successful viral replication. However, due to their limited coding capacity, viruses must enact most, if not all, of these metabolic changes by influencing the function of available host cell regulatory proteins. Typically, certain viral proteins, some of which can function as viral oncoproteins, interact with these cellular regulatory proteins directly in order to effect changes in downstream metabolic pathways. This review highlights recent research into how four different DNA tumor viruses, namely human adenovirus, human papillomavirus, Epstein–Barr virus and Kaposi’s associated-sarcoma herpesvirus, can influence host cell metabolism through their interactions with either MYC, p53 or the pRb/E2F complex. Interestingly, some of these host cell regulators can be activated or inhibited by the same virus, depending on which viral oncoprotein is interacting with the regulatory protein. This review highlights how MYC, p53 and pRb/E2F regulate host cell metabolism, followed by an outline of how each of these DNA tumor viruses control their activities. Understanding how DNA tumor viruses regulate metabolism through viral oncoproteins could assist in the discovery or repurposing of metabolic inhibitors for antiviral therapy or treatment of virus-dependent cancers.

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“…HBV induced metabolic dysregulation in heptitis has been investigated for many years, while the role of HBV in HCC metabolism remains unclear. It becomes more and more widely accepted that oncogenic DNA virus could hijack the cell metabolic machinery caused metabolic rearrangement sequentially [4].…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B Virus Associated Hepatocarcinoma Activated Unique Metabolism Pathway to Gain Survival Advantages

Zhao

Ning

Deng³

et al. 2021

Preprint

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Background: Hepatitis B Virus (HBV) is considered as a “metabolic virus” and affects the hepatic metabolism homeostasis, while except for the anti-virus therapy the principle of HBV-negtive hepatocellular carcinoma (HCC) and HBV-positive HCC is exactly the same until now. Exploration of the unique characteristics of HBV-associated HCC will provide new metabolic targets against HBV-associated HCC to gain survial advantage, and finally inhibit cancer progression. Methods: To systematically assess the metabolic changes, we assessed the transcriptomic and proteomic data from public database, additionally verified the accordingly changes in our own test cohort on proteome and transcriptome level. Additionally, the tissue metabolomics profile, lipidomics and the activity of PI3K/AKT/mTOR signaling pathway which play critical role in metabolism reprogramming, were analyzed to confirm the aforementioned changes. Results: By multi-omics approaches, we presented the metabolic dysfunction experienced during HBV-associated HCC, represented by upregulated the steroid hormone biosynthesis, primary bile acid, and sphingolipid metabolism which related to a poor prognosis. Metabolites in linoleic acid metabolism and primary bile acid metabolism were closely correlated with HBV replication in HBV-positive HCC patients. Further tissue metabolomics and lipidomics validate the serum metabolic changes, namely changing in lipid composition and unsaturated fatty acid accumulation. By antibody array, a hyperactive PI3K/AKT/mTOR signaling transduction in HBV-positive biopsy compared with HBV-negative patients was observed, indicating a key role of this pathway in metabolic reprogramming of HBV-associate HCC. Conclusion: HBV plays a critical role in the metabolism of HBV-associated HCC and activated a unique metabolism pathway to gain survival advantages. HBV-positive HCC showed obviously difference compared to HBV-negative HCC in metabolism at least and should be treated according to its characteristics in the clinic.

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From infection to cancer: how DNA tumour viruses alter host cell central carbon and lipid metabolism

Cited by 11 publications

References 90 publications

Identified lncRNAs functional modules and genes in prediabetes with hypertriglyceridemia by weighted gene co-expression network analysis

Identified lncRNAs functional modules and genes in prediabetes with hypertriglyceridemia by weighted gene co-expression network analysis

Metabolic Control by DNA Tumor Virus-Encoded Proteins

Hepatitis B Virus Associated Hepatocarcinoma Activated Unique Metabolism Pathway to Gain Survival Advantages

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