Zhiyong Zhang1, Yuanyuan Wang2, Xianxing Wang3, Hongguang Zhang4, Shuai Wang5. 1. Department of Neurosurgery, Caoxian People's Hospital Heze 274400, Shandong, China. 2. Department of Oncology, Linyi People's Hospital Linyi 251500, Shandong, China. 3. Department of Neurosurgery, Yuncheng County People's Hospital Heze 274700, Shandong, China. 4. Department of Neurosurgery, Gaotang People's Hospital Liaocheng 252800, Shandong, China. 5. Department of Neurosurgery, First Hospital of Zibo Zibo 255200, Shandong, China.
Abstract
OBJECTIVE: To illustrate the role of LRIG1 in regulating the Notch signaling pathway and glioma cell proliferation, apoptosis and invasion. METHODS: The glioma cells (U373) were divided into control group, NC group and LRIG1 group. After transfection, the CCK-8 assay, Transwell assay, and Flow cytometry were used to explore the biological function of LRIG1 in glioma cells. At the end, Western blot was used to detect the expression of LRIG1, Notch1, Hes1, Bcl-2, and Bax. RESULTS: The LRIG1 expression in U373 cells was remarkably lower than that in normal glial cells (P=0.019). The LRIG1 expression in the LRIG1 group was successfully increased when compared with that in the control group (P=0.004). The cell viability of the LRIG1 group was significantly lower than that of the NC group and control group at 24 h, 48 h, and 72 h (P=0.040, 0.025; P=0.041, 0.041; P=0.035, 0.035) respectively. Increased LRIG1 expression level in glioma cells strongly inhibits cell migration in transwell experiment. Flow cytometry results indicated that the apoptosis rate of the LRIG1 group was critically higher than that of the NC group and control group (P=0.003; P=0.003). According to results of Western blot, the expression levels of Notch1, Hes1, Hes5, and Jagged1 in LRIG1 group were dramatically higher than that in NC group and control group (P=0.006, 0.013; P=0.025, 0.026; P=0.001, 0.004; P=0.025, 0.027; P=0.029, 0.021) reespectively. While Bax expression in LRIG1 group was lower than that of NC group and control group (P=0.018, 0.021). CONCLUSION: The up-regulation of LRIG1 can inhibit the proliferation and migration of glioma cells and promote apoptosis by regulating the Notch signaling pathway. AJTR
OBJECTIVE: To illustrate the role of LRIG1 in regulating the Notch signaling pathway and glioma cell proliferation, apoptosis and invasion. METHODS: The glioma cells (U373) were divided into control group, NC group and LRIG1 group. After transfection, the CCK-8 assay, Transwell assay, and Flow cytometry were used to explore the biological function of LRIG1 in glioma cells. At the end, Western blot was used to detect the expression of LRIG1, Notch1, Hes1, Bcl-2, and Bax. RESULTS: The LRIG1 expression in U373 cells was remarkably lower than that in normal glial cells (P=0.019). The LRIG1 expression in the LRIG1 group was successfully increased when compared with that in the control group (P=0.004). The cell viability of the LRIG1 group was significantly lower than that of the NC group and control group at 24 h, 48 h, and 72 h (P=0.040, 0.025; P=0.041, 0.041; P=0.035, 0.035) respectively. Increased LRIG1 expression level in glioma cells strongly inhibits cell migration in transwell experiment. Flow cytometry results indicated that the apoptosis rate of the LRIG1 group was critically higher than that of the NC group and control group (P=0.003; P=0.003). According to results of Western blot, the expression levels of Notch1, Hes1, Hes5, and Jagged1 in LRIG1 group were dramatically higher than that in NC group and control group (P=0.006, 0.013; P=0.025, 0.026; P=0.001, 0.004; P=0.025, 0.027; P=0.029, 0.021) reespectively. While Bax expression in LRIG1 group was lower than that of NC group and control group (P=0.018, 0.021). CONCLUSION: The up-regulation of LRIG1 can inhibit the proliferation and migration of glioma cells and promote apoptosis by regulating the Notch signaling pathway. AJTR