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Anticancer Res ; 42(5): 2319-2326, 2022 May.
Article in English | MEDLINE | ID: mdl-35489746

ABSTRACT

BACKGROUND: α-Enolase (ENO1) is a glycolytic enzyme involved in the Warburg effect which cancer cells utilize to satisfy their higher need for nutrients. Up-regulation of ENO1 has been detected in several tumor types, including melanoma and endometrial, gastric and colorectal cancer. In these tumors, ENO1 may function as prognostic marker. Therefore, it was our interest to determine the expression of ENO1 in glioma and meningioma and whether chemotherapy of glioma alters ENO1 expression. MATERIAL AND METHODS: Tumor samples and control tissues were obtained during neurosurgery. All tumor samples were grouped according to WHO classification. Quantitative polymerase chain reaction and western blot were used to detect the expression of ENO1 in glioma and meningioma. All assays were carried out in triplicates; ß-actin was used as a housekeeping gene. For western blots, all samples were incubated with mouse monoclonal anti-ENO1 followed by secondary horseradish peroxidase-linked anti-mouse antibody, with ß-actin as a loading control. Immunofluorescence (n=33) was performed to determine the presence of ENO1 in tumor and control tissues using primary antibody to ENO1 and anti-Cy3 as secondary antibody. RESULTS: The expression of ENO1 mRNA was significantly higher in the control group compared to glioma (p<0.0001) and its protein was also significantly up-regulated in low-grade glioma in comparison to high-grade (p<0.0001). ENO1 expression in grade II and III meningiomas was increased compared to grade I (p=0.016 and p=0.0010, respectively) and in grade III compared to grade II (p=0.0363). CONCLUSION: Our findings suggest that ENO1 might be a marker for meningioma progression and that ENO1 is up-regulated in low-grade glioma.


Subject(s)
Glioma , Meningeal Neoplasms , Meningioma , Actins , Animals , Biomarkers, Tumor/genetics , DNA-Binding Proteins/genetics , Glioma/genetics , Glioma/pathology , Humans , Meningeal Neoplasms/genetics , Meningioma/genetics , Mice , Phosphopyruvate Hydratase/genetics , Tumor Suppressor Proteins/genetics
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