BRD7 Suppresses PD-L1 Expression to Counteract Immune Evasion in Nasopharyngeal Carcinoma
Abstract
Nasopharyngeal carcinoma (NPC) is a prevalent head and neck malignancy with unique epidemiological and clinical characteristics [1, 39]. Despite advances in treatment, immune evasion remains a significant challenge, often mediated by the overexpression of programmed death-ligand 1 (PD-L1) on tumor cells [2, 7, 8]. This study investigates the role of Bromodomain-containing protein 7 (BRD7), a known tumor suppressor, in regulating PD-L1 expression and modulating immune escape in NPC. We demonstrate that BRD7 is frequently downregulated in NPC and that its restoration significantly inhibits PD-L1 expression both in vitro and in vivo. Mechanistically, BRD7 exerts this effect by directly binding to the PD-L1 promoter, leading to transcriptional repression. Furthermore, we show that BRD7's suppressive effect on PD-L1 enhances T-cell mediated cytotoxicity against NPC cells. These findings reveal a novel mechanism by which BRD7 contributes to anti-tumor immunity in NPC, suggesting that strategies aimed at upregulating BRD7 or targeting its downstream effects could improve the efficacy of immunotherapy for NPC patients.
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