Fig. 10: EBV-miR-BART11 and EBV-miR-BART17-3p promote tumor escape in xenograft mice models. | Nature Communications

Fig. 10: EBV-miR-BART11 and EBV-miR-BART17-3p promote tumor escape in xenograft mice models.

From: EBV miRNAs BART11 and BART17-3p promote immune escape through the enhancer-mediated transcription of PD-L1

Fig. 10

a Bright-field images of transplanted tumors in the CDX nude mice models. The mice were sacrificed after 25 days of injection with the activated T cells. n = 8 per group. b Mechanism of EBV-miR-BART11 and EBV-miR-BART17-3p in the activation of PD-L1 and the promotion of tumor immune escape. EBV-encoded BART11 or BART17-3p target FOXP1 or PBRM1 to transcriptionally repress their expression, respectively. FOXP1 binds directly to the PD-L1 enhancer, whereas PBRM1 cannot directly bind to it. PBRM1 forms the PBAF complex and binds to FOXP1 to exert effects on the PD-L1 enhancer. The PBAF and BAF complexes compete with each other in assembly to bind with the PD-L1 enhancer to affect PD-L1 expression, resulting in tumor immune escape. Source data are provided as a Source Data file.

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