Glut-1 And Its Regulating Factor Hif-1 Alpha Expression In Epithelial Ovarian Tumors: Glut-1 Is Associated With Molecular Typing And Grade Of Epithelial Ovarian Cancer

Objective: Hypoxia plays an important role in tumorigenesis and tumor progression. Under the hypoxia environment, glucose uptake is increased to support the growth of tumor. Here we analyzed the expression of GLUT-1 and hypoxia inducible factor-1 alpha (HIF-1 alpha) in epithelial ovarian tumors, investigated the correlation between their expression and the molecular typing (Kurman's model) or histological grade of epithelial ovarian cancer. Then explore the possible significance of GLUT-1 in diagnosis and treatment of ovarian cancer. Materials and methods: 154 cases with primary epithelial ovarian tumors (malignant: 63 cases, borderline: 42 cases, benign: 49 cases) were studied. Immunohistochemistry was performed using GLUT-1 and HIF-1 alpha antibody. GLUT-1 protein expression was quantified by Western blot analysis. GLUT-1 mRNA expression was analyzed by real time PCR (RT-PCR). Results: Both of the expressions of GLUT-1 and HIF-1 alpha were increased gradually from benign to malignant ovarian tumors, they showed a sequence correlation. But, only GLUT-1 expression synchronously showed a statistical difference in molecular typing, histological grade and FIGO Stage of epithelial ovarian cancer (P<0.05). And there is a positive correlation between the expression of GLUT-1 and HIF-1 alpha, the correlation coefficient was 0.232 (P<0.05). At the same time, the expression pattern showed that as the score of GLUT-1 staining increased the intensity and extent of HIF-1 alpha expression was enhanced accordingly. Western blot and RT-PCR analysis were in accordance with the immunohistochemical staining of GLUT-1. Conclusion: Our study suggests that the expression of GLUT-1 was closely related with molecular typing and histological grade of epithelial ovarian cancer. GLUT-1 could be a novel diagnosis biomarker and therapeutic target for epithelial ovarian cancer.