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Human leukocyte antigen B (HLA-B), a novel member of the NF-kappaB signal pathway in laryngeal squamous cell carcinoma (LSCC), mediates immunological surveillance of tumor cells by presenting peptides to cytotoxic T-lymphocytes (CTLs) together with S100 calcium binding protein A8 (S100A8). The objective of this study was to investigate the molecular mechanism of HLA-B and S100A8 in laryngeal carcinogenesis. Flow cytometry, 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) assay and cell invasion in vitro were used to detect the biological effect of the Hep2 cell line induced by HLA-B RNA interference. RT-PCR and Western blotting were applied to evaluate the expression level of the S100A8 gene after HLA-B RNA interference. Our results showed that HLA-B had negative effects on Hep2 cells by inhibiting apoptosis and cell invasion while decreasing cell proliferation. Additionally, the expression level of HLA-B and S100A8 in LSCC were down-regulated after HLA-B RNA interference. The abnormal expression of HLA-B is thus relevant to the biological effect of laryngeal carcinoma and participates in the NF-kappaB signal pathway partly by regulating the expression of the S100A8 gene.

HLA-B gene participates in the NF-κB signal pathway partly by regulating S100A8 in the laryngeal carcinoma cell line Hep2