Zhang Zhiyong, Wang Yuanyuan, Wang Xianxing, Zhang Hongguang, Wang Shuai
Department of Neurosurgery, Caoxian People's Hospital Heze 274400, Shandong, China.
Department of Oncology, Linyi People's Hospital Linyi 251500, Shandong, China.
Am J Transl Res. 2022 Feb 15;14(2):788-797. eCollection 2022.
To illustrate the role of LRIG1 in regulating the Notch signaling pathway and glioma cell proliferation, apoptosis and invasion.
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.
The LRIG1 expression in U373 cells was remarkably lower than that in normal glial cells (=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).
The up-regulation of LRIG1 can inhibit the proliferation and migration of glioma cells and promote apoptosis by regulating the Notch signaling pathway.
阐明LRIG1在调节Notch信号通路以及神经胶质瘤细胞增殖、凋亡和侵袭中的作用。
将神经胶质瘤细胞（U373）分为对照组、阴性对照组（NC组）和LRIG1组。转染后，采用CCK-8法、Transwell法和流式细胞术探究LRIG1在神经胶质瘤细胞中的生物学功能。最后，采用蛋白质免疫印迹法检测LRIG1、Notch1、Hes1、Bcl-2和Bax的表达。
U373细胞中LRIG1的表达明显低于正常神经胶质细胞（P=0.019）。与对照组相比，LRIG1组中LRIG1的表达成功上调（P=0.004）。在24小时、48小时和72小时时，LRIG1组的细胞活力明显低于NC组和对照组（分别为P=0.040，0.025；P=0.041，0.041；P=0.035，0.035）。在Transwell实验中，神经胶质瘤细胞中LRIG1表达水平的升高强烈抑制细胞迁移。流式细胞术结果表明，LRIG1组的凋亡率显著高于NC组和对照组（P=0.003；P=0.003）。根据蛋白质免疫印迹法结果，LRIG1组中Notch1、Hes1、Hes5和Jagged1的表达水平分别显著高于NC组和对照组（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）。而LRIG1组中Bax的表达低于NC组和对照组（P=0.018，0.021）。
LRIG1的上调可通过调节Notch信号通路抑制神经胶质瘤细胞的增殖和迁移，并促进其凋亡。
