关键词: 脑胶质瘤, TRPM7, PI3K/AKT/ERK信号途径, 增殖, 上皮-间质转化

Abstract: Objective  To investigate the effect of silent melastatin transient receptor potential channel 7(TRPM7) on the proliferation and epithelial-mesenchymal transition of brain glioma cells and the underlying mechanism. Methods The TRPM7 expression in human normal astrocyte cell line HA1800 and glioma cell lines(U251, U87 and U373) were detected by qRT-PCR and Western blot. U251 cells were divided into the U251 group(untransfected U251 cells), U251/shNC group and U251/shTRPM7 group, then the expression of TRPM7 was detected by qRT-PCR and Western blot;  the cell proliferation ability was detected by cell clone formation assay;  the cell migration and invasion ability were detected by Transwell migration and invasion experiments;  the expression of E-cadherin and Vimentin was detected by cellular immunofluorescence assay;  the expression of PI3K/AKT/ERK signaling pathway-related proteins were detected by Western blot. Results Compared with HA1800 cells, TRPM7 was highly expressed in glioma cell lines(P<0.05). Silencing TRPM7 reduced the expression of TRPM7 in U251 cells(P<0.001), and the ability of cell proliferation, migration and invasion were significantly reduced(P<0.01);  E-cadherin expression was increased(P<0.001) and Vimentin expression was decreased(P<0.01);  the expression level of PI3K protein was down-regulated(P<0.01), and the phosphorylation level of AKT protein and ERK1/2 protein were also significantly reduced(P<0.01). Conclusion Silencing TRPM7 can inhibit the proliferation, migration, invasion ability and epithelial-mesenchymal transformation of U251 cells, which may be related to the PI3K/AKT/ERK signaling pathway.

Key words: Glioma, TRPM7, PI3K/AKT/ERK signaling pathway, Proliferation, Epithelial-mesenchymal transformation  ,