Sahar Ghasemi - Student research committee, Semnan University of Medical Sciences, Semnan, Iran
Ali Ghanbari - Research center of physiology, Semnan University of Medical Sciences, Semnan, Iran
Marjan Bahraminasab - Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran
Samaneh Arab - Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran

Background and aim: Glioblastoma Multiforme (GBM) is a type of brain cancer that is very aggressive and spreads rapidly. Furthermore, glioblastoma is extremely resistant to the majority of chemotherapeutic drugs and radiation therapy regimens, so the identification of novel molecular targets is highly essential to provide treatment choices for these patients. The function of CD۷۳, an enzyme that is involved in adenosine (ADO) generation, in glioblastoma development has been demonstrated however the details of its molecular mechanisms are not realized nevertheless. The purpose of the current project is to assess the effect of CD۷۳ molecule inhibitor (adenosine ۵′-(α, β-methylene) diphosphate (APCP) on angiogenesis process in experimental orthotopic glioblastoma.Materials and Methods: In vivo anti-angiogenic activity of APCP was studied using the C۶ glioblastoma model. ۳۰ Wister female rats In the weight range of ۲۰۰ to ۲۵۰ gr were randomly divided into three groups (APCP, vehicle (control) and untreated) , On days ۷, ۹, ۱۲, ۱۴, ۱۶, and ۱۸ after tumor induction, APCP (۴۰۰ μg/۲۰۰μl) or drug solvent (vehicle) (۲۰۰μl) were administered intraperitoneally. One day following the final injection, sacrificed and brains were harvested. Immunohistological evaluation was performed for CD۳۱ and VEGF protein expression.results: Immunohistochemical staining revealed the effective down-regulation of VEGF and CD۳۱ in the APCP group in contrast to the control (P≤۰/۰۵). It is also clear that the expression of these angiogenic inducing elements in both treated groups (control and APCP) was higher than in the untreated group (P≤۰/۰۵).Conclusion: In conclusion, our findings indicate that CD۷۳ inhibition can diminish tumor new vessel generation by inhibiting the molecules involved in this process, thereby CD۷۳ may be a practical target and provide novel opportunities for improving the treatment of malignant brain tumors.

Glioblastoma Multiforme (GBM), CD۷۳, Angiogenesis