MHC class I
peptide loading complex defects are frequently observed in
tumor cells which facilitate
tumor cells escaping from immune surveillance.
Tapasin plays an important role in the assembly of
MHC class I molecules with
peptides in the endoplasmic reticulum. The aim of this study was to investigate the expression of
tapasin in primary
oral squamous cell carcinoma (OSCC) and its potential clinical implication.
Formalin-fixed,
paraffin-embedded
tumor biopsies from 67 patients with primary OSCC were analyzed for
tapasin expression using immunohistochemistry.
Tapasin promoter methylation status in OSCC cell lines was determined using ethylation-specific polymerase chain reaction, bisulphate genomic sequencing, and expression reactivation assay. Lack of
tapasin expression was observed in 30 of 67 (43%)
tumors and was significantly associated with poor pathologic differentiation grade of OSCC (P = 0.028). The cumulative 5-year survival rate was also significantly correlated with pathologic differentiation grade (P = 0.001) and
tapasin expression level (P = 0.015). Decreased
tapasin expression was an
indicator of poor survival (P = 0.048).
Tapasin promoter methylation was observed in all three OSCC cell lines examined, and the
mRNA and
protein levels of
tapasin increased markedly
after treatment with
5-aza-2'-deoxycytidine. Downregulation of
tapasin is associated with a poor clinical outcome for OSCC patients and may serve as a prognostic
biomarker. The promoter methylation may contribute to the
tapasin downregulation in OSCC.