![]() Most HNSCC cases arise from the mucosal lining in the oral cavity, pharynx and larynx and can seriously limit the chewing ability, speech, cosmetology, and even life of patients. Head and neck cancer ranks as the sixth leading malignancy worldwide, with almost 90% of cases classified as head and neck squamous cell carcinoma (HNSCC). Our results suggest that lncMX1–215 negatively regulates immunosuppression by interrupting GCN5/H3K27ac binding in HNSCC, thus providing novel insights into immune checkpoint blockade treatment. Finally, overexpression of lncMX1–215 suppressed HNSCC proliferation and metastasis capacity in vitro and in vivo. Clinically, negative correlations between lncMX1–215 and PD-L1 and galectin-9 expression were observed. Mechanistically, we found that lncMX1–215 directly interacted with GCN5, a known H3K27 acetylase, to interrupt its binding to H3K27 acetylation. Binding sites for H3K27 acetylation were found on PD-L1 and galectin-9 promoters. Subsequently, histone deacetylase (HDAC) inhibitors promoted the expression of PD-L1 and galectin-9. Ectopic expression of lncMX1–215 markedly inhibited expression of the IFNα-induced, immunosuppression-related molecules programmed cell death 1 ligand 1 (PD-L1) and galectin-9, and vice versa. LncMX1–215 was primarily located in the cell nucleus. ![]() We identified a novel IFNα-induced upregulated lncRNA, lncMX1–215, in HNSCC. The role and mechanism of lncRNA in immunosuppression were investigated in HNSCC in vitro and in vivo. Methodsĭifferentially expressed lncRNAs were screened under IFNα stimulation using lncRNA sequencing. ![]() Interferon alpha (IFNα) is a well-established regulator of immunosuppression in head and neck squamous cell carcinoma (HNSCC), while the role of long noncoding RNAs (lncRNAs) in immunosuppression remains largely unknown.
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