OBJECTIVETo investigate the expression of STK15 and P53 proteins in oral precancerous lesions and oral squamous cell carcinoma (OSCC) and elucidate the possible role of P53/STK15 switch activation-independent pathway in oral carcinogenesis.

METHODSFormalin-fixed, paraffin-embedded tissues of 8 cases of normal oral epithelium, 27 cases of dysplasia with different degree epithelium dysplasia and 43 cases of OSCC with different differentiation were investigated for the expression of STK15 and P53 proteins by using immunohistochemistry. The clinical and pathological significance of STK15 over-expression in oral carcinogenesis were statistically analyzed by SPSS 12.0.

RESULTSSTK15 protein was not detectable in normal oral epithelium and significantly altered from mild-dysplasia to OSCC. The percentage of STK15 over-expression were 40.74% (11/27) in dysplasia and 67.44% (29/43) in OSCC (P < 0.05). The percentage of STK15 over-expression in OSCC with positive P53 staining was significantly higher than that in OSCC with negative P53 staining (P < 0.05). STK15 over-expression was significantly associated with regional lymph node involvement (P < 0.05), while no correlation was found for STK15 over-expression and tumor differentiation, as well as TNM stages.

CONCLUSIONSTK15 up-regulation was an early event in oral carcinogenesis. The up-regulation of STK15 protein in OSCC may partly result from p53 mutations, which probably contribute a role in lymph node metastasis of OSCC as well. P53/STK15 switch activation-independent pathway may play some roles in oral carcinogenesis.