Cancer-promoting function of lncRNA KCNQ1OT1 in colon cancer cells and its downstream regulatory pathways

Objective To clarify the function of IncRNA KCNQ1 OT1 in HCT-116 and HT-29 colon cancer cell lines,and explore the molecular mechanism of its role in colon cancer cells. Methods HCT-116 and HT-29 cells transfected by LncRNA KCNQ10 T1 overexpression plasmid and blank control served as pcDNA3.1-KCNQ1 OT1 group and pcDNA3.1 group,and the two cell lines cells knocked down by siRNA and blank control served as si-KCNQ1 OT1 group and NC group.CCK8,scratch assay,Trans well and cell invasion assay were conducted to verify the effect of lncRNA KCNQ1 OT1 on cell function.RNA immune Precipitation(RIP)assay and double luciferase labeling assay were applied to verify the binding interaction between KCNQ1 OT1 and miR-125 a-5 p and the binding interaction between miR-125 a-5 p and SMURF1.After overexpression and knockdown of KCNQ1 OT1 and miR-125 a-5 p,the expression of SMURF 1 was verified by western blot.Rescue experiment was performed to detect the expression of SMURF1 after co-transfection and co-knockdown of KCNQ1 OT1 and miR-125 a-5 p. Results In HCT-116 and HT-29 cells,overexpressed KCNQ1 OT1 could promote the proliferation,migration and invasion of colon cancer cells.After knockdown of KCNQ1 OT1,the proliferation,migration and invasion of colon cancer cells were inhibited.miR-125 a-5 p could specifically bind to both KCNQ1 OT1 and SMURF1.Overexpression of KCNQ1 OT1 promoted the expression of SMURP1,while knockdown of KCNQ1 OT1 inhibited the expression of SMURF1.Overexpression of miR-125 a-5 p inhibited the expression of SMURF1,and knockdown of miR-125 a-5 p promoted the expression of SMURF 1.On the basis of overexpression of KCNQ1 OT1,expression of miR-125 a-5 p could significantly inhibit the expression of SMURF1,while knockdown of miR-125 a-5 p and KCNQ1 OT1 could promote the expression of SMURF1. Conclusion In colon cancer cells,lncRNA KCNQ1 OT1 promotes the proliferation,migration and invasion of colon cancer cells by regulating the KCNQ10 T1-miR-125 a-5 p-SMURFl axis.