Signaling pathways of EBV-induced oncogenesis

Luo, Yin; Liu, Yitong; Wang, Chengkun; Gan, Runliang

doi:10.1186/s12935-021-01793-3

Cited by 56 publications

(62 citation statements)

References 92 publications

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“…The carcinogenic mechanisms of the HPV and the EBV viruses can be different [79][80][81], for example, the integration of the HPV genome is a critical stage in HPV carcinogenicity [82] while this phenomenon is not observed in EBV. Accumulating evidence suggests that both viruses contribute to tumor progression by affecting the common pathways.…”

Section: Discussionmentioning

confidence: 99%

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

et al. 2021

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Background This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. Methods This case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay. Results The EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18–45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Conclusion The HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors.

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Section: Discussionmentioning

confidence: 99%

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

et al. 2021

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“…The Janus tyrosine kinase and signal transducer and transcription activator pathway activated by LMP-1 mediates expression of programmed cell death protein ligand 1 aiding the cancer cells escape the body's immune surveillance. 17 LMP-1 makes more cells susceptible to the virus by secretion of matrix metalloproteases, which facilitate the degradation of the extracellular matrix. The stability of p53, a tumor suppressor gene, is interfered with by LMP-1, such that there is a lack of induced cell apoptosis in the cell cycle.…”

Section: Introductionmentioning

confidence: 99%

“…15 LMP-1 regulates a number of signaling pathways in the pathogenesis of NPC, mainly through the three functional domains of its C terminal activating regions 1, 2, and 3. 16,17 Through the NF-κB signaling pathway, LMP-1 regulates cell proliferation, apoptosis, transformation, metastasis, and invasion ultimately causing immortalization through the p65 subunit. LMP-1 plays a crucial role in the chemokine ligand 5-mediated cancer angiogenesis by activating the phosphoinositide 3-kinase protein kinase B (PI3K AKT) and hypoxia-inducible factor 1α signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Epstein-Barr Virus Latent Membrane Protein-1 Expression in Nasopharyngeal Carcinoma

Salano

Mwakigonja

Abdulshakoor

et al. 2021

JCO Global Oncology

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PURPOSE Nasopharyngeal carcinoma (NPC), a malignant neoplasm of the epithelium covering the nasopharynx, is a rare disease in most parts of the world. Epstein-Barr virus (EBV), the most potent oncogenic virus, coupled with environmental and genetic factors has been identified to play a role in the development of NPC. An array of methods for detecting the virus do exist, from serologic detection of antibodies to DNA amplification. There is paucity of local data on the status of EBV infection in relation to NPC within the region, and this study attempts to shed more light on the subject. METHODS This was a retrospective cross-sectional laboratory-based study on histologically confirmed, archived tissues from July 2015 to June 2019. Immunohistochemistry expression of latent membrane protein-1 (LMP-1) was used to detect EBV infection in the tissues. RESULTS A total of 71 cases were enrolled in this study. The mean age was 47.87 years ± 16.84 years with a male-to-female ratio of 1.5:1. There was a unimodal distribution of EBV detection, with the peak (26.8%) at 36-45 years. About 45.1% of the 71 samples tested positive for LMP-1, all of which were nonkeratinizing carcinoma. Nonkeratinizing carcinoma was the most common histopathologic subtype (n = 67; 94.4%), with the majority (38 of 67; 56.7%) being undifferentiated and 29 of 67 (43.3%) differentiated. Keratinizing and basaloid subtypes had two cases each, representing 2.8%. CONCLUSION A significant proportion of NPC, particularly nonkeratinizing histologic subtype, seems to show LMP-1 positivity by immunohistochemistry, which may be adopted in resource-constrained settings to detect EBV infection in these tissue biopsies.

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“…NF-κB dysregulation, among others, is a pivotal step in the occurrence and development of many tumors. The expression of NF-κB is upregulated in several cancers, including head and neck squamous cell carcinoma (HNSCC), pancreatic ductal adenocarcinoma, colorectal cancer, and gastric cancer [ 60 , 61 ]. The expression and activation of p65, the most well-studied NF-kB subunit in cancer, is increased in RCC tissues [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Epstein–Barr virus infection is associated with the nuclear factor-kappa B p65 signaling pathway in renal cell carcinoma

et al. 2022

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Background There have been few studies regarding viral involvement in the pathogenesis of renal cell carcinoma (RCC). The aim of this study was to examine the possible association of Epstein–Barr virus (EBV) infection with clinicopathological features and cellular biomarkers including p53, p16INK4a, Ki-67 and nuclear factor-kappa B (NF-κB) in RCC tumors. Methods In this prospective study, 122 histologically confirmed Formalin-fixed Paraffin-embedded RCC tissue specimens along with 96 specimens of their corresponding peritumoral tissues and 23 samples of blunt renal injuries were subjected to nested polymerase chain reaction (nPCR) in order to amplify EBV DNA sequences. The expression of p53, p16INK4a, Ki-67 and NF-κB was investigated by immunohistochemistry (IHC) assay. Statistical analysis was employed to demonstrate the possible associations. Results Infection with EBV was found to be significantly associated with RCC. Our results indicate that p65 NF-κB signaling pathway is probably involved in EBV-mediated RCC pathogenesis. Moreover, we found p53, Ki-67 and cytoplasmic NF-κB expression to be associated with tumor nuclear grade in RCC patients. The expression of p53 and Ki-67 was associated with primary tumor category as well. In addition, p53 overexpression was significantly more frequent among nonconventional RCC tumors than the conventional histologic type. Conclusions Infection with EBV is likely to play an important role in the development of RCC through the constitutive and permanent activation of NF-κB p65 signaling pathway. However, more experiments and supporting data are required to reach a decisive conclusion.

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Signaling pathways of EBV-induced oncogenesis

Cited by 56 publications

References 92 publications

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

Epstein-Barr Virus Latent Membrane Protein-1 Expression in Nasopharyngeal Carcinoma

Epstein–Barr virus infection is associated with the nuclear factor-kappa B p65 signaling pathway in renal cell carcinoma

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