
Dysregulated Epiregulin (EREG) promotes PDL1 upregulation in head and neck squamous cell carcinoma (HNSCC) via the c-myc pathway. N-glycosylation of EREG at N47, mediated by STT3B glycosyltransferases, is crucial for its stability and function. Mutation at N47 or STT3B knockdown destabilizes EREG, reducing PDL1 levels. Inhibiting STT3B with NGI-1 degrades EREG and suppresses PDL1. Combining NGI-1 with anti-PDL1 therapy enhances immunotherapy efficacy in HNSCC, highlighting STT3B-mediated glycosylation as a target for improving cancer treatment.
Like
Save
Share