4.4 Article

Effects of mir-128a on the invasion and proliferation of glioma U251 cells

Journal

ONCOLOGY LETTERS
Volume 17, Issue 1, Pages 891-896

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2018.9651

Keywords

mir-128a; glioma; U251 cells; invasion; proliferation; apoptosis

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Effects of mir-128a on the proliferation and migration of human glioma U251 cells were explored. The constructed mir-128a-shRNA lentivirus vector (infection group) and scramble shRNA (interference group) were transfected into glioma U251 cells, and uninfected U251 cells as control group. The expression level of mir-128a, the ability of proliferation, invasion, apoptosis and migration of cells in each group were detected by RT-qPCR, MTT assay, Transwell migration in vitro, cell wound scratch assay and TUNEL cell apoptosis assay. The expression level of mir-128a in U251 cells of infection group was significantly higher than that in U251 cells of interference group (P<0.05). he expression level of mir-128a in U251 cells of control group was significantly lower than that in U251 cells of infection group (P<0.05). The OD values of infection and control group were lower than that of interference group at 6, 12, 24, 48 and 72 h, and the OD values of infection were lower than that of control group at 6, 12, 24, 48 and 72 h (P<0.05). Compared with infection and control group, the number of membrane-penetrating cells in U251 cells of interference group increased significantly (P<0.05). The apoptosis rate of U251 cells of infection and control group was significantly higher than that of interference group, and the apoptosis rate of infection was significantly higher than that of control group (P<0.05). The migration distance of U251 cells of infection and interference group was significantly larger than that of control group (P<0.05). he migration distance of U251 cells of interference group was significantly larger than that of infection group (P<0.05). mir-128a may play a role similar to anti-oncogene in glioma, inhibiting the ability of proliferation, invasion and migration of glioma cells, and promoting the apoptosis of glioma cells.

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