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.