Promotes the Development of Glioma by Ubiquitination and Degradation of .

OBJECTIVE

To investigate the effect of on glioma cells and further explore its underlying molecular mechanisms.

METHODS

Mouse xenograft model was used in this study. The mRNA expression of was detected by qRT-PCR. The cell viability and proliferation activity was detected by MTT assay and colony formation assay. The migration and invasion of glioma cells were determined by Transwell assay. The protein levels of , FOXO1, CyclinD1, C-myc, MMP-2 and TIMP-1 were assessed by Western-blotting. The interaction between TRIM47 and FOXO1 was measured by Co-immunoprecipitation (Co-IP) assay.

RESULTS

In glioma tissues and cells, was significantly up-regulated. Silencing the expression of inhibited the cell viability and proliferation of cells A172 and U251, as well as their ability to invade and migrate. Among them, the expression levels of C-myc and CyclinD1 also decreased, and MMP-2 was down-regulated and TIMP-1 was up-regulated. Similarly, in vivo model, tumor volume and weight also decreased after knockout. Further research showed that TRIM47 inhibited expression by ubiquitination and degradation of , thereby promoting glioma growth and progression.

CONCLUSION

In our study, we confirmed functional role of the axis in the progression of gliomas and provided a potential target for glioma treatment.