Taken together, our data firstly demonstrated that CREB1-induced FOXD2-AS1 contributed to glioma progression by upregulating AKT1 via competitively binding to miR-185, providing a novel strategy for targeting FOXD2-AS1 as a potential biomarker and a therapeutic target in glioma patients.
Our experiments mainly reveal that the CREB1 could affect glucose transport in glioma cells by regulating the expression of GLUT1, which controlled the metabolism of glioma and affected the progression of glioma.
These results indicate that miR-200b targets the CREB1 gene and suppresses glioma cell growth, suggesting that miR-200b shows tumor-suppressive activity in human malignant glioma.