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
Weili Zheng, Guilan Lai, Ziyuan Liao, Jianzhen Shen
TL;DR
A new long noncoding RNA called lncADEI helps Epstein-Barr virus-positive lymphoma grow and avoid the immune system by boosting PD-L1.
Contribution
The study identifies lncADEI as a novel lncRNA that promotes EBV+ DLBCL progression and immune evasion via the miR-93-3p/STAT3/PD-L1 axis.
Findings
LncADEI is upregulated in EBV+ DLBCL and promotes cell proliferation and clonogenesis.
LncADEI activates STAT3 via miR-93-3p, which increases PD-L1 expression and immune evasion.
LncADEI is present in serum exosomes of EBV+ DLBCL patients and correlates with poor outcomes.
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…
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Taxonomy
TopicsCancer-related molecular mechanisms research · Viral-associated cancers and disorders · Extracellular vesicles in disease