The Relationship between the Cell Proliferation and miR-107by Targeting Sall4in Human Glioma
|School||Harbin Institute of Technology|
|Keywords||hsa-miR-107 Sall4 glioma proliferation|
MicroRNAs can regulate gene expression via interacting with target gene. Sall4was detected significantly up-regulated in many tumors, as a new oncogene to belearned. But the mechanism of the regualation on it is not clear. Our previous workhas shown that Sall4was up-regulated in human glioma tissues, and predicted Sall4was the target gene of has-miR-107by bioinformatics method. Using a luciferasereporter system, real-time RT-PCR and western blot, SALL4was identified as noveldirect target of miR-107in cells. To gain a better understanding of the regulation onSall4, we detected the expression of miR-107and Sall4mRNA in40human gliomatissues by qRT-PCR. The results tured out that30of40(75%) cases revealed lessthan50%down-regulation by detected the expression of miR-107, and31of40(77.5%)cases revealed more than50%up-regulation by detected the expression ofSall4. An obvious inverse correlation was observed between the expression ofmiR-107and Sall4by analysis software.Forced expression of miR-107suppressed cell proliferation by MTT assay andan anchorage-independent growth assay in SHG-44, U251and U87-MG cells. Inaddition, miR-107could induce apoptosis by FACS and caspase3/7activity assay.The nude mice were injected with SHG-44cells which were transfected withmiR-107mimics in their backside region, and we found that the proliferation abilityof the cells was remarkably reduced.Then the apotosis was detected in the thesection of tumors by TUNEL assay, which shown that forced expression of miR-107can aslo induce cell apotosis compared with the control group in vivo.To conclude, miR-107can inhibit the proliferation of glioma cells by inducingapotosis in vitro and vivo.