Effect of lncrna zeb1-as1 on proliferation, invasion and apoptosis of glioma u87 cells

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Abstract

This study aimed to investigate the effect of LncRNA ZEB1-AS1 on the proliferation, invasion and apoptosis of human glioma U87 cells. U87 glioma cells were divided into three groups. The Si group was transfected with LncRNA ZEB1-AS1 specific SiRNA. The NC group was transfected with non-specific scramble siRNA, and untransfected glioma cells were used as the blank group. After 48 h of transfection, the proliferation of U87 cells was detected by MTT assay, apoptosis of U87 cells was detected by flow cytometry, and Transwell invasion assay was used to detect cell invasion. The expression of LncZEB1-AS1 in Si group was significantly lower than that in the NC and blank groups (P<0.01). There was no statistical difference in the OD 490 between the three groups at 24 h (P>0.05). At 48 h, the Si group was significantly lower than the NC group and the blank group (P<0.01). After 48 h, the three groups showed a gradually increasing trend, but at all the time points, the Si group was always lower than the NC and blank groups (P<0.01). The OD values of the blank and NC groups were significantly higher than the same group at the previous time point (P<0.01). The OD values of Si group at 48 and 96 h were significantly higher than those at the previous time point (P <0.05). Although there was an upward trend between 72 and 48 h, the difference was not significant (P>0.05). Flow cytometry detected apoptosis in each group and found that the apoptosis rate in the Si group was significantly higher than that in the NC and blank groups (P<0.01). Inhibition of LncRNA ZEB1-AS1 can inhibit the proliferation and invasion of glioma U87 cells and promote apoptosis. LncRNA ZEB1-AS1 is expected to become a new target for the treatment of glioma.

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CITATION STYLE

APA

Zhang, W., & Xiong, L. (2019). Effect of lncrna zeb1-as1 on proliferation, invasion and apoptosis of glioma u87 cells. Oncology Letters, 17(6), 5120–5124. https://doi.org/10.3892/ol.2019.10202

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