Correlation of survivin and B-cell lymphoma 2 expression with pathological malignancy and anti-apoptotic properties of Glial cell tumors

Abstract

Apoptosis, whose mechanism remains unclear, is regulated by multiple factors. B-cell lymphoma 2 (Bcl-2) is a well-known anti-apoptotic mediator. Survivin is also a recently recognized novel family inhibitor of apoptosis protein, which inhibits apoptosis via a pathway distinct from Bcl-2 family members. Survivin and Bcl-2 are expressed in various types of human cancer. In the present study, survivin and Bcl-2 expression were characterized in glial cell tumors, and the correlation with pathological malignancy and anti-apoptotic properties were investigated. Fifty-eight patients who had undergone surgical resection for glial cell tumors were evaluated. The pathological types of glial cell tumors were categorized according to the World Health Organization classification. Survivin and Bcl-2 expression levels were investigated by western blot 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 survivin and Bcl-2 or co-expression. 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 the tumor specimens. Survivin expression in astrocytic tumors was identified to be significantly associated with the pathological grade (P<0.05); however, Bcl-2 was not (P>0.05). Anti-apoptotic rate of glial cell tumors were detected in 91.4, 92.0 and 100% of patients exhibiting survivin, Bcl-2 or co-expression, respectively. However, the difference in anti-apoptotic frequency between the three groups was not identified to be statistically significant (P>0.05). The present study suggests that survivin expression is correlated with pathological grades of gliomas. In addition, the expression of survivin or Bcl-2 exerts potent anti-apoptotic properties in gliomas. Thus, survivin or Bcl-2 may serve as potential targets for inducing the apoptosis of gliomas.