舒尼替尼调控miR-143对人肾癌细胞增殖、侵袭的影响

目的:探讨miR-143在肾癌细胞中的作用、舒尼替尼对miR-143表达的影响及与细胞增殖、侵袭的关系.方法:培养人肾癌786-O细胞株,分为对照组、miR-143组、舒尼替尼组、共同作用组.对照组细胞转染阴性对照序列,miR-143组细胞转染miR-143序列,舒尼替尼组细胞用舒尼替尼处理48 h,共同作用组细胞转染...

Effect of regulation of miR-143 by sunitinib on the proliferation and invasion of human renal carcinoma cells

ObjectiveTo investigate the role of miR-143 in renal cell carcinoma, the effect of sunitinib on the expression of miR-143 and its association with cell proliferation and invasion.MethodsThe human renal carcinoma 786-O cells were divided into control group, miR-143 group, sunitinib group and co-action group.The negative control sequence was transfected into the cells of control group, the miR-143 sequence was transfected into the cells of miR-143 group, sunitinib group cells were treated with sunitinib for 48h, the co-acting group was transfected miR-143 sequence and treated with sunitinib for 48h.Proliferation and invasion of 786-O cells were detected by MTT and transwell experiment, miR-143 RNA expression was detected by qRT-PCR, DNA methyltrans-ferase3B(DNMT3B).The expressions of p-Akt-S473 protein were detected by Western blotting.ResultsThe human renal cancer 786-O cells with stable and high expression of miR-143 were successfully constructed.The expression of miR-143 was increased in the miR-143 transfected group(P < 0.01).The IC₅₀ value in 786-O cells with the treatment of sunitinib for 48 h was 6 μmol/L, which was selected as the drug concentration in the subsequent experiment.The expression of miR-143 in 786-O cells was increased after the treatment of sunitinib for 48 h(P < 0.01).Cell survival rate, cell invasion number, expressions of DNMT3B and p-Akt-S473 protein in miR-143 and sunitinib group were all lower than control group and higher than co-action group(P < 0.05 to P < 0.01).ConclusionsmiR-143 reduced the proliferation and invasion capacity of 786-O cells, which may be related to the decreased expression of DNMT3B and p-Akt regulated by miR-143.Sunitinib may inhibit the proliferation and invasion of 786-O cells by upregulating miR-143.