Function and mechanism of miR-23 a-3 p in the brain gliomas

Objective: To investigate the expression of miR-23a-3p in human glioma tissues and its effects on the growth of glioma as well as the proliferation, migration, cell cycle and apoptosis of U251 cells. Methods: The intracellular gene expression level was detected by qPCR. CCK8 was used to detect the cell proliferation. Transwell assay was adopted to detect cell migration. Flow cytometry was used to detect the cell cycle and apoptosis. And the targeted regulation of miR-23a-3p to the CTNNBIP1 was detected by dual-luciferase test. Results: In glioma, miR-23a-3p expression level was proportional to the malignant degree of glioma and the expression level in HGG (high grade glioma) was significantly higher than that of LGG (lower grade glioma); correspondingly, the expression of CTNNBIP1 was inversely proportional to the malignant glioma degree and the expression level in HGG was lower than that of LGG. Analyzing the correlation between miR-23a-3p and CTNNBIP1, we found there was negative correlation between the two. The dual-luciferase experiment confirmed that the two were targeting, and miR-23a-3p could target regulate the expression of CTNNBIP1. The lentivirus transfection technique was used to interfere the expression of miR-23a-3p in the cells and analyze the function of miR-23a-3p in the U251 cells. It was found that the down regulation of miR-23a-3p expression suppressed the proliferation, migration, cell cycle, and promoted l apoptosis of U251 cells. On the basis of the interference of miR-23a-3p, we interfered the expression of CTNNBIP1, then find that compared with interference of miR-23a-3p group, the cells inhibition of proliferation, migration and cycle had been weakened; however, the effect on promoting apoptosis had been inhibited. The nude mice in vivo experiment confirmed that the low expression of CTNNBIP1 can reduce the expression of miR-23a-3p and the inhibitory effect on tumor growth worked. Conclusion: miR-23a-3p is defined as oncogene in glioma, which can promote the development of glioma cells. And this promotion effect is achieved by targeting CTNNBIP WNT pathway to inhibit synthesis of protein.