Long non-coding RNAs (lncRNAs) regulate gene expression at the epigenetic, transcriptional, or posttranscriptional level by interacting with protein, DNA, and RNA. Emerging evidence suggests that various lncRNAs are abnormally expressed and play indispensable roles in virus-triggered cancers. Besides, a growing number of studies have shown that virus-encoded lncRNAs participate in tumorigenesis. However, the functions of most lncRNAs in tumors caused by oncogenic viruses and their underlying mechanisms remain largely unknown. In this review, we summarize current findings regarding lncRNAs involved in cancers caused by Epstein–Barr virus (EBV) and Kaposi’s sarcoma herpesvirus (KSHV). Additionally, we discuss the contribution of lncRNAs to tumor occurrence, development, invasion, and metastasis; the roles of lncRNAs in key signaling pathways and their potential as biomarkers and therapeutic targets for tumor diagnostics and treatment.

Exosomes are extracellular membrane vesicles with a diameter of 30–100 nm, produced by different eukaryotic cells that contain multitudinous lipids, nucleic acids, and proteins. They transfer membrane components and nucleic acids between cells, thereby performing an information exchange between cells. Many studies have shown that a variety of tumor-associated viruses can exert their biological functions through exosomes. The tumor microenvironment (TME) is very important in the occurrence, development, and chemoresistance of tumors. It is composed of tumor cells, fibroblasts, endothelial cells, immune cells, stromal cells, and acellular components, such as exosomes and cytokines. This review focuses on the effects of virus-related components secreted by tumor cells over the TME in several virus-associated cancers.

Increasing evidence shows that Epstein-Barr virus (EBV) infection is closely related to various lymphoid and epithelioid malignancies. However, the underlying mechanisms are unclear. GCNT3 (core 2β-1,6-acetylglucosaminyltransferase) is a new type of core mucin synthase, and its expression in EBV-associated gastric cancer (EBVaGC) is lower than that in EBV-negative gastric cancer (EBVnGC). EBV-encoded latent membrane protein 2A (LMP2A) is a transmembrane protein with tumorigenic transformation properties. Here, we demonstrated that LMP2A inhibited the transcription of GCNT3 by inhibiting Smad2/3 and Smad4. LMP2A restrained the activation of the mTORC1 pathway by inactivating the TGF-β1/Smad pathway and then downregulated GCNT3 expression. The mTORC1-GCNT3 pathway promoted cell proliferation and migration and inhibited G0/G1 cell arrest. Related proteins involved in epithelial-mesenchymal transition (EMT) were downstream molecules of the TGF-β1/Smad-mTORC1-GCNT3 pathway. GCNT3 inhibited autophagy by inducing mTORC1 phosphorylation. These findings indicate that targeting the TGF-β1/Smad-mTORC1-GCNT3 axis may represent a novel therapeutic target in GC. Importance Epstein-Barr virus (EBV) is an opportunistic pathogen, and the latent membrane protein 2A (LMP2A) encoded by EBV plays a key role in ensuring the incubation period of EBV. Glycosylation modification is an important marker of cancer cells, and recent studies have reported that it is related to EBV. Our conclusions provide deeper theoretical support for the role of LMP2A and TGF/Smad-mTORC1-GCNT3 in EBVaGC and help to understand glycosylation abnormalities in cancer. Our results may provide novel therapeutic targets for the treatment of gastric cancer against the TGF/Smad-mTORC1-GCNT3 signaling cascade.

Epstein-Barr virus (EBV) is the first virus to be known to have direct association with human cancer and to be considered as an important DNA tumor virus. The EBV life cycle consists of both latent and lytic modes of infection in B lymphocytes and epithelial cells.

Aim: To investigate the role of AHR in nasopharyngeal carcinoma (NPC) and explore the relationship between Epstein–Barr virus (EBV) infection and the AHR pathway. Methods: The effect of LMP1 on the expression of AHR was analyzed using real-time PCR and western blot. Proliferation and migration of cells were assessed using CCK8 and Transwell analysis. Results: EBV infection downregulated the expression of AHR in NPC cells, possibly through activation of the ERK pathway by LMP1 thereby accelerating AHR proteasomal degradation following translocation to the nucleus. Cell proliferation, migration and autophagy are promoted by activating the AHR pathway. Conclusion: In NPC cells, LMP1 increases the phosphorylation of ERK, which may activate the AHR pathway.

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