Metabolic reprogramming: a hallmark of viral oncogenesis

Lévy, Pierre; Bartosch, Birke

doi:10.1038/onc.2015.479

Cited by 46 publications

(40 citation statements)

References 178 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Energy metabolism is crucial for cell proliferation, differentiation, migration, and survival (26). Most cancer cells rely on the Warburg effect as a source of ATP.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐31‐5p enhances the Warburg effect via targeting FIH

et al. 2018

View full text Add to dashboard Cite

The enhanced expression of miR-31 has been observed in many human malignancies including lung cancer, and this microRNA regulates several aspects of oncogenesis. However, the role of miR-31-5p in energy metabolism remains elusive. Here, we confirm that H1299 and A549 cells, 2 lung cancer cell lines, relay on aerobic glycolysis as main source of ATP. Inhibition of miR-31-5p leads to decreased glycolysis and ATP production, while miR-31-5p overexpression increases them. Hypoxia inducible factor 1 (HIF-1) up-regulates the expression of glycolytic enzymes, and the HIF-1α inhibitor (FIH) inhibits HIF-1 activity. Because FIH is a direct target of miR-31-5p, inhibition of miR-31-5p results in enhanced FIH expression and suppression of HIF-1 signaling, while overexpression of miR-31-5p has the opposite effects. Via this mechanism, miR-31-5p up-regulates aerobic glycolytic genes and maintains energy homeostasis. To further validate the mechanism of miR-31-5p in glycolysis regulation, we show that overexpression or knockdown of FIH rescued the effects of miR-31-5p or miR-31-5p inhibitor on HIF activation and its target gene expression, respectively. Finally, by means of an A549 cell xenograft mouse model, we demonstrate that the miR-31-5p promotes cell proliferation via enhancing glycolysis. In summary, this study reveals that miR-31-5p promotes the Warburg effect via direct targeting of FIH.-Zhu, B., Cao, X., Zhang, W., Pan, G., Yi, Q., Zhong, W., Yan, D. MicroRNA-31-5p enhances the Warburg effect via targeting FIH.

show abstract

“…Energy metabolism is crucial for cell proliferation, differentiation, migration, and survival (26). Most cancer cells rely on the Warburg effect as a source of ATP.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐31‐5p enhances the Warburg effect via targeting FIH

et al. 2018

View full text Add to dashboard Cite

show abstract

“…As intracellular parasites, viruses depend on the metabolism of infected cells to proliferate. To avoid metabolic exhaustion, viruses manipulate metabolic pathways and associated signalling cascades to provide sufficient resources to support the optimal production of virions, which indicates that metabolic reprogramming is a hallmark of viral oncogenesis27. Copeland et al .…”

Section: Discussionmentioning

confidence: 99%

Multi-omics analyses reveal metabolic alterations regulated by hepatitis B virus core protein in hepatocellular carcinoma cells

Xie

Fan

Wei

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Chronic hepatitis B virus (HBV) infection is partly responsible for hepatitis, fatty liver disease and hepatocellular carcinoma (HCC). HBV core protein (HBc), encoded by the HBV genome, may play a significant role in HBV life cycle. However, the function of HBc in the occurrence and development of liver disease is still unclear. To investigate the underlying mechanisms, HBc-transfected HCC cells were characterized by multi-omics analyses. Combining proteomics and metabolomics analyses, our results showed that HBc promoted the expression of metabolic enzymes and the secretion of metabolites in HCC cells. In addition, glycolysis and amino acid metabolism were significantly up-regulated by HBc. Moreover, Max-like protein X (MLX) might be recruited and enriched by HBc in the nucleus to regulate glycolysis pathways. This study provides further insights into the function of HBc in the molecular pathogenesis of HBV-induced diseases and indicates that metabolic reprogramming appears to be a hallmark of HBc transfection.

show abstract

“…It leads to the elevation of glucose influx into the lymphocytes, monocytes, and epithelial cells. Enhanced glucose flux is known to promote infection with oncogenic viruses [154, 155]. In case of HIV-1, it also leads to augmented ROS production and enhanced infection of target cells [147, 156, 157].…”

Section: Ros In Hiv's Life Cyclementioning

confidence: 99%

Oxidative Stress during HIV Infection: Mechanisms and Consequences

Ivanov

Valuev-Elliston

Иванова

et al. 2016

Oxidative Medicine and Cellular Longevity

272

246

View full text Add to dashboard Cite

It is generally acknowledged that reactive oxygen species (ROS) play crucial roles in a variety of natural processes in cells. If increased to levels which cannot be neutralized by the defense mechanisms, they damage biological molecules, alter their functions, and also act as signaling molecules thus generating a spectrum of pathologies. In this review, we summarize current data on oxidative stress markers associated with human immunodeficiency virus type-1 (HIV-1) infection, analyze mechanisms by which this virus triggers massive ROS production, and describe the status of various defense mechanisms of the infected host cell. In addition, we have scrutinized scarce data on the effect of ROS on HIV-1 replication. Finally, we present current state of knowledge on the redox alterations as crucial factors of HIV-1 pathogenicity, such as neurotoxicity and dementia, exhaustion of CD4+/CD8+ T-cells, predisposition to lung infections, and certain side effects of the antiretroviral therapy, and compare them to the pathologies associated with the nitrosative stress.

show abstract

Metabolic reprogramming: a hallmark of viral oncogenesis

Cited by 46 publications

References 178 publications

MicroRNA‐31‐5p enhances the Warburg effect via targeting FIH

MicroRNA‐31‐5p enhances the Warburg effect via targeting FIH

Multi-omics analyses reveal metabolic alterations regulated by hepatitis B virus core protein in hepatocellular carcinoma cells

Oxidative Stress during HIV Infection: Mechanisms and Consequences

Contact Info

Product

Resources

About