微小RNA-218-5p靶向三磷酸腺苷结合盒超家族G家族第2个成员基因对人口腔鳞状细胞癌细胞增殖、迁移和侵袭的影响

Effects of MicroRNA-218-5p Targeting ABCG2 Gene on Proliferation,Migration,and Invasion of Tca-8113 Cells

目的:研究微小RNA(microRNA,miR)-218-5p靶向调控三磷酸腺苷结合盒超家族G家族第2个成员(ATP-binding cassette sub-family G member 2,ABCG2)基因对Tca-8113细胞的增殖、迁移和侵袭的影响,并探讨其机制。方法:运用实时荧光定量聚合酶链反应(quantitative Real-time PCR,qRT-PCR)与Western blot检测Tca-8113细胞和NOK细胞中miR-218-5p和ABCG2的表达。通过双荧光素酶报告基因实验检测miR-218-5p和ABCG2靶向关系。用脂质体法将miR-218-5p mimic、ABCG2小干扰RNA(interfering RNA,siRNA)、miR-218-5p mimic+pcDNA-ABCG2分别转染至Tca-8113细胞中,噻唑蓝(methyl thiazol tetrazolium,MTT)法、Transwell法检测Tca-8113细胞的增殖、迁移和侵袭。结果:与NOK细胞比较,Tca-8113细胞miR-218-5p呈显著低表达,ABCG2呈显著高表达(P<0.05)。过表达miR-218-5p、抑制ABCG2均可抑制Tca-8113细胞的增殖和迁移(P<0.05)。双荧光素酶报告基因实验证实miR-218-5p与ABCG2的靶向结合关系。过表达ABCG2可逆转上调miR-218-5p对Tca-8113细胞增殖、迁移和侵袭的抑制作用。结论:上调miR-218-5p的表达可靶向调控ABCG2,抑制Tca-8113细胞的增殖、迁移和侵袭,将可为口腔鳞状细胞癌的治疗提供新的靶点。

Objective:To investigate the effects of miR-218-5p targeting ABCG2 gene on the proliferation,migration,and invasion of Tca-8113 cells and its mechanism.Methods:qRT-PCR and western blot were used to detect the expression of miR-218-5p and ABCG2 in Tca-8113 and NOK cells.The targeting relationship between miR-218-5p and ABCG2 was detected by dual luciferase reporter gene experiment.miR-218-5p mimic,ABCG2 siRNA and miR-218-5p mimic+pcDNA-ABCG2 were transfected into Tca-8113 cells by liposome method.The proliferation,migration,and invasion of Tca-8113 cells were detected by MTT and Transwell tests.Results:Compared with NOK cells,miR-218-5p was significantly down-regulated in Tca-8113 cells,and ABCG2 was significantly expressed(P<0.05).Over-expression of miR-218-5p and inhibition of ABCG2 inhibited proliferation and migration of Tca-8113 cells(P<0.05).There is a targeted binding relationship between miR-218-5p and ABCG2.Over-expression of ABCG2 reverses the inhibitory effect of up-regulated miR-218-5p on proliferation,migration,and invasion of Tca-8113 cells.Conclusion:Up-regulating the expression of miR-218-5p can target ABCG2 to inhibit the proliferation,migration,and invasion of Tca-8113 cells,which may provide a new target for the treatment of OSCC.