Objective To observe the effect of overexpression of a long noncoding RNA (LncRNA) LINC00152 on the tumor growth of human glioma U251 tumor-bearing mice and to explore its related mechanisms. Methods Lentiviral transfection upregulated the expression of LINC00152 in U251 cells. LINC00152 overexpression (LV-LINC00152 group) and empty control (LV group) cells were established, and normal U251 cells were used as the blank group (Control group). qRT-PCR was used to detect the expression of LINC00152. A U251 tumor-bearing mouse model was established. The p-YAP inhibitor XMU-MP-1 was administered to mice and the tumor volume was measured and the tumor weight was weighed at the end of the experiment. Immunohistochemical staining was used to observe the expression of Ki67 in tumor tissues. The expressions of YAP, p-YAP, LATS1 and p-LATS1 proteins were detected by Western blotting. Results Compared with the LV group, the expression of LINC00152 in the LV-LINC00152 group was significantly upregulated ( P < 0. 01). End of experiment, compared with the LV tumor-bearing mice, the tumor volume and tumor weight in the LVLINC00152 group were increased significantly ( P <0. 01). XMU-MP-1 (1 and 3 mg/ kg) treatment significantly reduced the tumor volume and tumor weight of LV-LINC00152 tumor-bearing mice in a dose-dependent manner ( P <0. 01). Ki67 staining in the LV group was weakly positive but strongly positive in the LV-LINC00152 group. After XMU-MP-1 (1 and 3 mg/ kg) treatment, Ki67 was weakly positive in the tumor tissues of the LV-LINC0015 group. Compared with the LV group, the expression of p-YAP and p-LATS1 protein in the LV-LINC00152 group was significantly upregulated ( P <0. 01), and XMU-MP-1 (1 and 3 mg/ kg) treatment reversed the p-YAP and p-LATS1 protein expression ( P <0. 01). Conclusions The long noncoding RNA LINC00152 induces YAP phosphorylation to promote glioma growth, while the p-YAP inhibitor XMU-MP-1 inhibits the above biological effects of the long noncoding RNA LINC00152.