ArticleCell death & disease2026
Long noncoding RNA ADEI/miR-93-3p/STAT3 axis promotes Epstein-Barr virus-positive diffuse large B-cell lymphoma progression and immune evasion through regulating the PD-1/PD-L1 checkpoint.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Epstein-Barr virus (EBV) is an important pathogenic factor of lymphoma; EBV+diffuse large B-cell lymphoma (DLBCL) has a worse prognosis with standard chemotherapy than EBV-DLBCL. Long noncoding (Lnc)-RNAs are key regulators of cancer pathways and biomarkers of disease. As natural protective carriers of noncoding RNAs, exosomes can stably transmit signals during tumor development. We explored the role of exosomal lncRNAs in the occurrence and development of EBV-related DLBCL. In this study, we identified a novel lncRNA lncADEI, which was upregulated in EBV + DLBCL and was positively correlated with DLBCL cell proliferation and clonogenesis. LncADEI positively regulated STAT3 via miR-93-3P, and STAT3 transcriptionally activated programmed death ligand-1 to promote immune evasion of DLBCL cells. LncADEI could be transferred by exosomes and promote the proliferation and immune evasion of DLBCL. LncADEI was highly expressed in serum exosomes from EBV + DLBCL patients and was associated with worse clinicopathological features. In conclusion, lncADEI participated in the progression and immune evasion of EBV + DLBCL and was differentially expressed in serumal exosomes. LncADEI may be a promising strategy for treating EBV-associated lymphoid malignancies.
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