P04.63 ENO1 ist downregulated in meningiomas and upregulated in low grade gliomas

BACKGROUND: Cancer cells reorganize their metabolic pathways to gain nutrients such as glucose and glutamine because of their anabolic needs. Anaerobic glycolysis increases the total glycolysis in hypoxic conditions and normal oxygen conditions, which is known as the “Warburg effect”. The α-Enolase (ENO1), a glycolytic enzyme, produces ATP, through converting 2-phosphoglycerat to phosphoenolpyruvate and contributes to the “Warburg effect”. In various tumors as breast cancer, pancreatic cancer and gastric cancer the expression of ENO1 is augmented. The aim of the study is to examine whether ENO1 is also higher expressed in gliomas and meningiomas. It was also of interest whether the therapy with temozolomide in gliomas changes the concentration of ENO1. MATERIAL AND METHODS: To determine the expression of ENO1 in meningiomas, qPCR and Western Blots were performed. All experiments were done in triplicates.ß-Actin and MRLP19 were used as reference genes. The meningioma samples were sorted in grad I, grade II, grade III. Non-tumorous brain tissue was used as control group. The protein level of ENO1 in glioma were measured through Western Blot. The glioma samples used were sorted in non-tumorous brain tissue, grade II, grade III, secondary and primary glioblastoma with and without temozolomide. All samples used for Western Blots were incubated with mouse monoclonal anti-ENO1 antibody. A secondary HPR-linked anti-mouse antibody was used to make the lanes visible. ß-Actin was used as a loading control antibody. RESULTS: The qPCR data showed a higher ENO1 expression in control samples than grade I meningioma (5.6 ± 2.403 vs. 2.907 ± 1.931, p= 0.002). In grade II and III the concentration was higher compared to grade I (4.994 ± 2.064 vs. 2.907 ± 1.931, p= 0.002; 4.98 ± 2.385 vs 2.907 ± 1.931vs, p= 0.01). The Western Blot data showed a higher ENO1 concentration in control samples than in meningioma tissues (control: 1.262 ± 0.256 vs. grade I: 1.037 ± 0.16, p=0.047; control vs. grade II: 0.961 ± 0.119, p= 0.012; control vs. grade III: 0.966 ± 0.1311, p= 0.015). Western Blots showed an upregulation of ENO1 in grade II gliomas compared to all groups (2.00 ± 0.66 vs. control: 1.00 ± 0.247, p=0.0031; vs. grade III: 1.173 ± 0.369, p= 0.010; vs. secondary GBM: 0.902 ± 0.199, p= 0.0006). Secondary GBM had lower ENO1 concentration than treated secondary GBM (0.902 ± 0.199 vs. 1.231 ± 0.199, p=0.021). An enhanced expression could be seen in treated secondary GBM compared to treated primary GBM (1.231 ± 0.199 vs. 0.902 ± 0.1336, p= 0.029). CONCLUSION: In meningiomas no difference was found between the different grades on the posttranslational level. However, ENO1 level was lowered in meningiomas compared to healthy tissue. Grade II gliomas showed higher ENO1 expression than high grade gliomas. This data suggests that ENO1 could play a role in brain tumors.