ArticleFrontiers in immunology2026
Mechanism by which SAHA regulates HLA-E expression via the endoplasmic reticulum stress-related PERK/ATF4/CHOP pathway in neuroblastoma.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Human leukocyte antigen E (HLA-E) plays a role in tumor immune escape and is associated with poor prognosis in neuroblastoma (NB). This study aimed to investigate the regulatory effect of suberoylanilide hydroxamic acid (SAHA) on HLA-E expression via the PERK/ATF4/CHOP pathway in NB. Methods: A high HLA-E expression model in NB cells was established by stimulation with interferon-gamma (IFN-γ). The effects of SAHA on NB cell proliferation and migration were evaluated. In addition, the influence of SAHA on the PERK/ATF4/CHOP signaling pathway and HLA-E expression at the mRNA and protein levels was analyzed. Bioinformatics analysis was performed using data from the TARGET and Gene Expression Omnibus (GEO; GSE85047) databases to identify prognostic genes associated with NB. Results: Stimulation with IFN-γ successfully induced high HLA-E expression in NB cells. SAHA significantly suppressed NB cell proliferation and migration and downregulated HLA-E expression at both the mRNA and protein levels. Analysis of the TARGET database revealed that the prognosis of patients with NB was closely related to the expression levels of endoplasmic reticulum stress (ERS)-related proteins, particularly PERK and HLA-E. This association was validated using the GEO dataset GSE85047. Moreover, SAHA inhibited the expression of ERS pathway proteins, including PERK and CHOP, in NB cell lines. Conclusion: This study demonstrated that SAHA downregulates HLA-E expression by inhibiting the PERK/ATF4/CHOP pathway, offering new insights into the regulation of tumor proliferation, migration, and immune evasion in NB.
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