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Published on: September 7, 2022
EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis
Tingting Yang1, Chanping You2, Shuhui Meng3
1Department of Pharmacy, Shenzhen University General Hospital, Shenzhen, China.
Abstract:
Viral oncogenes may drive cellular metabolic reprogramming to modulate the normal epithelia cell malignant transformation. Understanding the viral oncogene-mediated signaling transduction dysregulation that involves in metabolic reprogramming may provide new therapeutic targets for virus-associated cancer treatment. Latent EBV infection and expression of viral oncogenes, including latent membrane proteins 1 and 2 (LMP1/2), and EBV-encoded BamH I-A rightward transcripts (BART) microRNAs (miR-BARTs), have been demonstrated to play fundamental roles in altering host cell metabolism to support nasopharyngeal carcinoma (NPC) pathogenesis. Yet, how do EBV infection and its encoded oncogenes facilitated the metabolic shifting and their roles in NPC carcinogenesis remains unclear. In this review, we will focus on delineating how EBV infection and its encoded oncoproteins altered the metabolic reprograming of infected cells to support their malignances. Furthermore, based on the understanding of the host's metabolic signaling alterations induced by EBV, we will provide a new perspective on the interplay between EBV infection and these metabolic pathways and offering a potential therapeutic intervention strategy in the treatment of EBV-associated malignant diseases.
Insights
Epstein-Barr virus (EBV) infection reprograms host cell metabolism via viral oncogenes like LMP1/2 and miR-BARTs. This metabolic shift fuels nasopharyngeal carcinoma (NPC) development, offering potential therapeutic targets for EBV-associated cancers.
Area of Science:
- Molecular biology
- Oncology
- Virology
- Metabolic pathways
Background:
- Viral oncogenes can induce cellular metabolic reprogramming, crucial for malignant transformation.
- Epstein-Barr virus (EBV) infection, particularly latent EBV, is linked to nasopharyngeal carcinoma (NPC).
- Key EBV oncoproteins, including latent membrane proteins 1 and 2 (LMP1/2) and EBV-encoded BamH I-A rightward transcripts (BART) microRNAs (miR-BARTs), are implicated in altering host cell metabolism.
Purpose of the Study:
- To elucidate the mechanisms by which EBV infection and its oncogenes mediate metabolic reprogramming in host cells.
- To understand the role of EBV-induced metabolic alterations in the pathogenesis of nasopharyngeal carcinoma (NPC).
- To explore potential therapeutic strategies targeting metabolic pathways in EBV-associated malignancies.
Main Methods:
- Review of existing literature on EBV, oncogenes, and cellular metabolism.
- Analysis of signaling transduction pathways dysregulated by viral oncogenes.
- Focus on metabolic shifts induced by EBV oncoproteins (LMP1/2, miR-BARTs) in NPC pathogenesis.
Main Results:
- EBV infection significantly alters host cell metabolism through its oncogenes.
- Specific viral oncoproteins (LMP1/2, miR-BARTs) play critical roles in driving these metabolic changes.
- Metabolic reprogramming supports the malignant transformation and progression of NPC.
Conclusions:
- EBV-driven metabolic reprogramming is a key factor in NPC development.
- Understanding these metabolic alterations provides insights into virus-associated cancer pathogenesis.
- Targeting EBV-induced metabolic pathways presents a promising therapeutic avenue for EBV-associated cancers.
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