Correlation of Survivin and Bcl-2 expression to pathological malignancy and anti-apoptotic property in glial cell tumors

Abstract

Objective Apoptosis, its mechanism remained unclear, is regulated by multiple factors. Bcl-2 is a well-known anti-apoptotic mediator. Survivin is also a recently recognized noble family inhibitor of apoptosis protein (IAP), which inhibits apoptosis through a pathway distinct from Bcl-2 family members. Survivin and Bcl-2 have been expressed in several human cancers. We characterized survivin and Bcl-2 expression in glial cell tumors, and investigated correlation to pathological malignancy and anti-apoptotic property. Methods Fifty-eight patients who had been surgically resected glial cell tumor were evaluated in this study. The pathological types of glial cell tumors were categorized according to World Health Organization classification (WHO). Survivin and Bcl-2 were investigated by Western blotting analysis, and apoptosis was detected by DNA fragmentation analysis. The anti-apoptotic rate of glial cell tumors was calculated in tumor samples according to the expression of the survivin and Bcl-2 or co-expression.

Results Survivin was characterized in 60.3%, and Bcl-2 was expressed in 43.1% of glioma samples. Co-expression of survivin and Bcl-2 was observed in 25.9% of tumor specimens. Survivin expression in astrocytic tumors was significantly associated with pathological grade (p < 0.05); however, Bcl-2 was not (p > 0.05). Anti-apoptosis in patients with survivin, Bcl-2, or co-expression was detected in 91.4%, 92.0%, and 100%, respectively. It demonstrated a high statistical significance, separately. However, the difference of anti-apoptotic frequency among 3 groups was not statistically significant (p > 0.05).

Conclusions These studies suggest that survivin expression has a correlation to pathological grades of gliomas. In addition, expression of survivin or Bcl-2 also has a potent anti-apoptotic property in gliomas. Our results indicate that survivin or Bcl-2 may be potential targets to induce apoptosis of gliomas.