Competing lncRNA XIST mediates the function of miR‐125b‐2‐3p by targeting WEE1. (A) Correlation of WEE1 and lncRNA XIST. The r values and P values are from Pearson's correlation analysis. (B) Real‐time qPCR quantification of WEE1 after the knockdown of lncRNA XIST. (C) Western blot of WEE1 in the total lysates of HCT116 cells transfected with miR‐125b‐2‐3p mimic, inhibitor, lncRNA XIST si#1, lncRNA XIST si#3 or control siRNA. (D) Representative images (left) and quantification (right) of cell viability in the indicated cells treated with or without 30 µM oxaliplatin for 48 h. The cells were transduced with the WEE1 lentivirus, mimic of miR‐125b‐2‐3p, or with si#1+si#3 to knock down lncRNA XIST; the cell apoptosis was measured with flow cytometry (n = 3). (E) PDX tumors were treated with or without oxaliplatin, and the tumor volumes were measured at each time point (n = 5). (F) WEE1 protein levels in HCT116 cells following the ectopic expression of miR‐125b‐2‐3p and/or knockdown of lncRNA XIST and/or overexpressed WEE1. (G) Proposed working model of this study. MiR‐125b‐2‐3p was absorbed by lncRNA XIST and regulated the expression of the WEE1, thus influencing the cell cycle. Data are presented as the mean ± SD. *
p < 0.05 or **
p < 0.01 versus the control