ArticleCancer science2021
Epstein-Barr virus latent membrane protein-1 upregulates autophagy and promotes viability in Hodgkin lymphoma: Implications for targeted therapy.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Mycobacterial antigen Ag85B restrains Hodgkin lymphoma tumor growth by inhibiting autophagy.Oncology research · 2025Article
- Epstein-Barr virus-driven molecular pathogenesis of primary pulmonary lymphoepithelial carcinoma.Frontiers in oncology · 2025Review
- Exploring the interplay between EBV and autophagy-related gene expression patterns in nasopharyngeal carcinoma.Frontiers in oncology · 2025Article
- [Mechanism by which mycobacterial antigen 85B inhibits autophagy and promotes apoptosis in Hodgkin lymphoma cells].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Chemotherapy's effects on autophagy in the treatment of Hodgkin's lymphoma: a scoping review.Discover oncology · 2024Article
- EBV and Lymphomagenesis.Cancers · 2023Review
- High percentages of peripheral blood T-cell activation in childhood Hodgkin's lymphoma are associated with inferior outcome.Frontiers in medicine · 2022Article
- Epstein-Barr virus latent membrane protein-1 upregulates autophagy and promotes viability in Hodgkin lymphoma: Implications for targeted therapy.Cancer science · 2021Article
- Activation of MEK1/2/Nrf-2 Signaling Pathway by Epstein-Barr Virus-Latent Membrane Protein 1 Enhances Autophagy and Cisplatin Resistance in T-Cell Lymphoma.Analytical cellular pathology (Amsterdam) · 2021Article
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Authors and funding
9 authors at 7 institutions in 2 countries.
Funding
Abstract
Hodgkin lymphoma (HL) is composed of neoplastic Hodgkin and Reed-Sternberg cells in an inflammatory background. The neoplastic cells are derived from germinal center B cells that, in most cases, are infected by Epstein-Barr virus (EBV), which may play a role in tumorigenesis. Given that EBV-latent membrane protein 1 (LMP1) regulates autophagy in B cells, we explored the role of autophagy mediated by EBV or LMP1 in HL. We found that EBV-LMP1 transfection in HL cells induced a modest increase in autophagy signals, attenuated starvation-induced autophagic stress, and alleviated autophagy inhibition- or doxorubicin-induced cell death. LMP1 knockdown leads to decreased autophagy LC3 signals. A xenograft mouse model further showed that EBV infection significantly increased expression of the autophagy marker LC3 in HL cells. Clinically, LC3 was expressed in 15% (19/127) of HL samples, but was absent in all cases of nodular lymphocyte-predominant and lymphocyte-rich classic HL cases. Although expression of LC3 was not correlated with EBV status or clinical outcome, autophagic blockade effectively eradicated LMP1-positive HL xenografts with better efficacy than LMP1-negative HL xenografts. Collectively, these results suggest that EBV-LMP1 enhances autophagy and promotes the viability of HL cells. Autophagic inhibition may be a potential therapeutic strategy for treating patients with HL, especially EBV-positive cases.
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