Author/Authors :
Chen، نويسنده , , Lingchao and Zhang، نويسنده , , Anling and Li، نويسنده , , Yongli and Zhang، نويسنده , , Kailiang and Han، نويسنده , , Lei and Du، نويسنده , , Wenzhong and Yan، نويسنده , , Wei and Li، نويسنده , , Ruiyan and Wang، نويسنده , , Yongzhi and Wang، نويسنده , , Kun and Pu، نويسنده , , Peiyu and Jiang، نويسنده , , Tao and Jiang، نويسنده , , Chuanlu and Kang، نويسنده , , Chunsheng، نويسنده ,
Abstract :
MicroRNAs are strongly implicated as affecting glioma, but their specific roles and functions have yet to be fully elucidated. In this study, we defined the expression and function of miR-24, which we found to be upregulated in glioma samples and glioma cells by qRT-PCR. Downregulation of miR-24 in glioma cell lines inhibited proliferation and invasion and induced apoptosis. Using computational and expression analysis, ST7L was identified as a candidate target of miR-24. A reporter assay with the 3′UTR of ST7L cloned downstream of a luciferase gene showed increased luciferase activity in the absence of miR-24, providing strong evidence that miR-24 is a direct regulator of ST7L. Furthermore, we observed that restoration of ST7L activity resulted in effects that were similar to those from transfecting a miR-24 inhibitor into glioma cells. Mechanistic investigation revealed that the deletion of miR-24 suppressed β-catenin/Tcf-4 transcription activity by targeting ST7L. In conclusion, our study demonstrates that miR-24 upregulation is common in glioma and that suppression of miR-24 expression inhibits cell proliferation and invasion, suggesting that miR-24 may act as an oncogene in glioma.
Keywords :
?-catenin , Tcf-4 , ST7L , Glioma , miR-24