UCHL1 enhances the malignant development of glioma via targeting GAS2.

Abstract

To detect the expression pattern of UCHL1 in glioma samples and its influence on the metastasis of glioma, as well as the underlying mechanism. UCHL1 levels in 42 paired glioma tissues and paracancerous ones were detected. The relationship between UCHL1 level and pathological indexes in glioma patients was analyzed. After establishing UCHL1 knockdown model in U251 and T98-G cells, their migratory ability was assessed by transwell and wound healing assay. At last, Luciferase assay, Western blot and rescue experiments were conducted to explore the role of UCHL1 in aggravating the development of glioma through targeting GAS2. UCHL1 was upregulated in glioma samples than paracancerous ones. High level of UCHL1 indicated high rates of lymphatic metastasis and distant metastasis, as well as low rates of overall survival and progression-free survival in glioma. Knockdown of UCHL1 markedly inhibited migratory ability in glioma cells. GAS2 was the downstream gene of UCHL1. A positive correlation was found between expression levels of UCHL1 and GAS2 in glioma tissues. Overexpression of GAS2 could reverse the inhibitory effects of silenced UCHL1 on migratory ability in glioma cells. UCHL1 level is linked to lymphatic metastasis, distant metastasis and prognosis in glioma patients. It stimulates migratory ability in glioma by positively regulating GAS2 level.