AKR1C2 small interfering RNA (siRNA) inhibited beta-catenin expression and transcriptional activation in human liver cancer cell line QGY7701.

Background/Aims: It has been proved that changes in the Wnt/β-catenin pathway lead to hepatocarcinogenesis and the AKR1C2 gene may contribute to the occurrence, advancement and invasiveness of liver cancer. The purpose of this study is to investigate AKR1C2 small interfering RNA (siRNA) influence on p-catenin expression and transcriptional activation in the human liver cancer cell line QGY7701. Methodology: We constructed AKR1C2 small interfering RNA (siRNA) expression vector pSilence2.1/ U6 /AKR1C2 RNAi and then transfected it into the liver cancer cell QGY7701. p-catenin mRNA and its protein expression was detected by RT-PCR, western blotting and p-catenin gene transcriptional activity was analyzed by luciferase assay. Results: AKR1C2 siRNA inhibited the transcriptional expression of P-catenin and decreased P-catenin protein stability in QGY7701. AKR1C2 siRNA inhibited P-catenin gene transcriptional regulation and control activity for TCF gene by influencing on the down-stream gene's function of P-catenin in QGY7701 liver cancer cells. Conclusions: It suggests a causative cooperative role for P-catenin and AKR1C2 in tumorigenesis. Thus, the inhibition of activation of the p-catenin/ TCF-signaling pathway is believed to be one mechanism by which AKR1C2 siRNA exerts a gatekeeper function during hepatocarcinogenesis.