Role of STK15/p53 pathway and centrosome amplification in oral squamous cell carcinomas / 中国肿瘤临床

ABSTRACT

Objective: This study proposed a possible molecular mechanism underlying centrosome amplification in oral squa-mous cell carcinoma (OSCC) by analyzing the relationship of centrosome amplification with the expression of STK15 and p53 in OS-CC tissues. Methods: The expression of STK15 and p53 in formalin-fixed, paraffin-embedded tissues from 8 patients with normal oral epithelium and 43 with OSCC were quantitatively analyzed by immunohistochemistry. Centrosome status was investigated by an indi-rect-immunofluorescence double-staining method to determine the message of centrosome amplification in OSCC. The correlation of the expression of the two proteins with centrosome amplification in OSCC was statistically analyzed with SPSS13.0. Results: Normal oral epithelium showed normal centrosomes in epithelium cells, whereas 33 of the 43 OSCC cases (76.74%) showed evidence of centro-some amplification. STK15 was undetectable in normal oral epithelium. The percentage of STK15 overexpression was 67.44% in OS-CC (P=0.028). The percentage of STK15 overexpression was significantly higher in OSCC with positive p53 staining than in OSCC with negative p53 staining (P=0.01). Spearman correlation analysis indicated a correlation between STK15/p53 positive co-expression and centrosome amplification of OSCC (P=0.019). Conclusion: Centrosome amplification is a common abnormal phenomenon in OS-CC. The p53/STK15 trans-activation-independent pathway plays a role in the systemic molecular regulation of centrosome in OSCC, which leads to the occurrence of OSCC.